Harmful health effects of exposure to “Forever Chemicals”

Harmful health effects of exposure to “Forever Chemicals”

OVERVIEW

  • Per- and polyfluoroalkyl substances (PFAS) are added to a variety of products (e.g., cosmetics, food packaging, non-adhesive cookware) to make them resistant to heat, water, oil and corrosion.
  • These “Forever Chemicals” are found in tap water, bottled water and in the blood of almost everyone in the West.
  • The presence of PFAS in the blood has been associated with higher risks of developing hypertension and type 2 diabetes in women.
  • PFAS are possibly associated with several health problems, including preeclampsia, impaired liver enzymes, increased blood lipids, decreased response to vaccines, and low birth weight.

Per- and polyfluoroalkyl substances (PFAS) are widely used in industrial and everyday consumer products, such as cosmetics, food packaging, non-adhesive cookware and floor coverings. PFAS contain extremely stable chemical bonds between fluorine and carbon atoms (F–C bonds), hence their pun-like nickname “Forever Chemicals” (see Figure 1). PFAS should not be confused with phthalates, another class of industrial products potentially harmful to health (see our article on the subject). It should be noted that another class of “Forever Chemicals” related to PFAS, hydrofluorocarbons or HFCs, are used to replace CFCs in refrigerants since they do not affect the ozone layer, but they are now being gradually withdrawn from the market since they are still greenhouse gases.

Figure 1. Structure of 3 per- and polyfluoroalkylated substances (PFAS) used in everyday consumer products.

PFAS are added to a host of products to make them resistant to heat, water, oil and corrosion. For example, the wrappers in which burgers, pizzas, salads, and other take-out food are wrapped contain PFAS, which helps prevent oil or dressing leaks. PFAS can migrate into food, especially when it contains a lot of fat and salts. In addition, the packaging is ultimately buried in landfills where there is the possibility of contaminating the soil and groundwater or, if they are incinerated, they can end up in the air. Consumer Reports tested more than 100 packaging products used in US restaurants and supermarkets and found PFAS in several products such as wrapping paper for french fries, hamburgers, disposable plates, and moulded fibre salad bowls. Further testing by Consumer Reports found that PFAS are present in tap water and bottled water in the United States. PFAS were detected in the blood of 98% of Americans tested.

During the first 60 years of PFAS production, many believed that the potential adverse effects only affected workers exposed to these products at an industrial level and not the general population. That was until in 1998 a farmer in Virginia in the United States started sounding the alarm about the effects of pollution produced by a DuPont factory on the health of his cows. Perfluorooctanoic acid (PFOA, also known as “C8”) may have affected approximately 70,000 people who got their water from the same contaminated source, according to the ensuing class action lawsuit in US courts. A committee set up to examine the dangerousness of PFOA subsequently established probable links between exposure to this product and several diseases, including thyroid disease, hypercholesterolemia, kidney and testicular cancer, pregnancy-induced hypertension, and ulcerative colitis.

Three PFAS (PFOS, PFOA and LC-PFCAs) are now banned in Canada because of the risk they pose to human health and the environment. It appears that the new PFAS that are being used today as replacements for the banned PFAS could also be harmful to human health and the environment. Therefore, the Government of Canada is considering regulating the use of all PFAS. PFAS are associated with several health problems, including preeclampsia, impaired liver enzymes, increased blood lipids, decreased response to vaccines, and low birth weight (see profile report of PFAS by the US Agency for Toxic Substances and Disease Registry).

Cosmetics
PFAS have been found in the ingredient list of several dozen cosmetic products sold in Europe and Asia, where they are added to make foundations, mascaras and liquid lipsticks more durable, waterproof and easier to spread. In a recent study, where more than 231 North American cosmetic products (including 21 from Canada) were analyzed, 52 products had a high fluorine content, indicating the presence of PFAS in high concentration. The presence of PFAS was confirmed in 29 products by mass spectrometry. Most of these cosmetic products, however, did not mention PFAS in the list of ingredients on the label. PFAS have been found particularly in products advertised as “long-lasting” or “wear-resistant”. Specifically, high levels of fluorine (from PFAS) were detected in 82% of water-resistant mascaras, 58% of other eye cosmetics (eye shadows and creams, eyeliner), 63% of foundations, and 62% of lipsticks. Among the 17 Canadian cosmetic products considered in the study, only one indicated the presence of PFAS in the list of ingredients.

Why are PFAS found in cosmetic products when they are not included in the list of ingredients? Some basic ingredients such as mica and talc can be treated with PFAS to improve their durability. Other ingredients such as acrylates, methicone, and other silicone polymers can be purchased in a form containing PFAS. It therefore seems that some cosmetic manufacturers use ingredients containing PFAS, yet don’t include them in the list of ingredients. It is best to avoid as much as possible using cosmetic products containing PFAS as they can be harmful to health and the probability of absorption through the skin is very high. The results of the study show that there are cosmetic products containing very little or no fluoride (and therefore PFAS), but they are difficult to identify since PFAS are not included in the ingredient lists of most cosmetic products. It is recommended to avoid using products advertised as “water-resistant”, “long-lasting” or “wear-resistant” which are likely to contain PFAS.

Hypertension
A prospective study found an unfavourable association between blood PFAS concentration and the risk of hypertension. The data comes from the Study of Women’s Health Across the Nation-Multi-Pollutant Study (SWAN-MPS) with 1058 middle-aged, normotensive women at baseline, who were followed from 1999 to 2017. During these years, 470 women became hypertensive (systolic pressure ≥140 mmHg or diastolic pressure ≥90 mmHg). Women who had the highest concentrations of PFOS, PFOA and EtFOSAA (a precursor to PFOS) in their blood had 42%, 47% and 42% higher risks, respectively, of developing hypertension compared to those who had the lowest concentrations of these PFAS. Women who had the highest concentrations of total PFAS had a 71% higher risk of developing hypertension. No significant association was observed for the following PFAS: perfluorononanoic acid (PFNA) and perfluorohexanesulfonic acid (PFHxS).

Type 2 diabetes
The same research group that conducted the study on the association between PFAS and the risk of hypertension also evaluated the association with the incidence of type 2 diabetes. The prospective study was conducted among 1237 women in the SWAN-MPS cohort who were 45-56 years old and nondiabetic at the start of the study (1999). During the study period (18 years), 102 women became diabetic. The latter had higher blood concentrations of PFAS than the non-diabetic women. Women who had high levels of PFAS in their blood were more likely to be black, to smoke or have smoked cigarettes, to be menopausal, or to have a higher body mass index (BMI). However, the data were adjusted to take into account several confounding factors, including race/ethnicity, place of residence, level of education, smoking, alcohol consumption, total energy intake, physical activity, menopause, and BMI.

Women who had the highest concentrations of n-PFOA, PFHxS, sm-PFOS and MeFOSAA in the blood had 67%, 58%, 36% and 85% higher risks, respectively, of developing type 2 diabetes compared to those with the lowest concentrations of these PFAS. Women who had the highest concentrations of four common PFAS (n-PFOA, PFNA, PFHxS and total PFOS) had a 64% higher risk of developing type 2 diabetes.

How to reduce exposure to PFAS?
PFAS have many important applications and eliminating them completely seems out of the question. The most problematic PFAS (PFOA, PFOS and LC-PFCAs) are no longer used in Canada. PFOA was used, among other things, for the manufacture of kitchen accessories with Teflon coating. The major problem with accessories containing Teflon is not that they release PFOA during use (very low level), but that their manufacture can release this “Forever Chemical” into the environment. Ceramic coatings and anodized aluminum are good alternatives. If the demand for kitchen accessories containing PFAS decreases, production will decrease and less of these substances will end up in the environment. Fast food wrapped in waterproof packaging or containers, cosmetics and body care products that contain PFAS should be avoided as much as possible, especially “water-resistant” or “wear-resistant” cosmetics. These are simple actions that can reduce exposure to these products that are potentially harmful to health.

Phthalates: A component of certain plastics and cosmetic products harmful to human health

Phthalates: A component of certain plastics and cosmetic products harmful to human health

OVERVIEW

  • Phthalates are chemicals added to plastics to make them more flexible and to some cosmetics to preserve their fragrance.
  • A certain amount of these products are released into the environment, including in food and beverages sold in some plastic containers.
  • Due to their widespread use, phthalates are ingested or absorbed without our knowledge and metabolites of these products are found in most people.
  • Phthalates are endocrine and metabolic disruptors, which are associated with adverse effects on neurodevelopment, childhood asthma, type 2 diabetes, ADHD, childhood and adult obesity, breast and uterine cancer, endometriosis and infertility.
  • Exposure to high-molecular weight phthalates, such as DEHP, has been associated with increased cardiovascular and all-cause mortality.
  • Voices are being raised in the scientific community for the use of phthalates to be subject to stricter regulations.

Phthalates are part of a class of chemicals that are widely used in industry (see Table 1 and Figure 1). High-molecular weight phthalates, such as di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP), are used as plasticizers to impart flexibility to polyvinyl chloride (PVC) materials used to make food packaging, flooring, and medical equipment (tubing, blood bags). Low-molecular weight phthalates, such as diethyl phthalate (DEP) and dibutyl phthalate (DBP), are added to shampoos, lotions and other personal care products to preserve their fragrance.

Since these phthalates are not chemically bound to plastics, they are released into the environment over time and can enter the human body by ingestion, inhalation and absorption through the skin. Once in the body, phthalates are rapidly metabolized and excreted in urine and faeces, so that half of the phthalates are eliminated within 24 hours of entering the body. Despite this rapid elimination, the population is permanently exposed to phthalates since these products are present in consumer products used almost every day. Metabolites of the phthalates DEHP and DiNP are detected in 98% of the total United States population. Daily exposure to a widely used phthalate, DEHP, has been estimated to range from 3 to 30 µg/kg/day, or 0.21 mg to 2.1 mg per day for a person weighing 70 kg (154 lb.).

Table 1. Main phthalates used in consumer products.   Adapted from Zota et al., 2014.

PhthalateAbbrev.Restricted use in the United StatesCommon sources
Low-molecular weight
Dimethyl phthalateDMPInsect repellents, plastic bottles, food
Diethyl phthalateDEPPerfumes, deodorants, cosmetics, soaps
Di-n-butyl phthalateDnBP++Cosmetics, medications, food packaging, food, PVC applications
Diisobutyl phthalateDiBPCosmetics, food, food packaging
High-molecular weight
Butylbenzyl phthalateBBzP++PVC flooring, food, food packaging
Dicyclohexyl phthalateDCHPFood, food packaging
Di(2-ethylhexyl) phthalateDEHP++PVC applications, toys, cosmetics, food, food packaging, blood bags, catheters
Di-n-octyl phthalateDnOP+PVC applications, food, food packaging
Diisononyl phthalateDiNP+PVC applications, toys, flooring, wall covering
Diisodecyl phthalateDiDP+PVC applications, toys, wires and cables, flooring

 

Figure 1. Chemical structure of the phthalates most commonly used in industry.

 

Phthalates and cardiovascular and all-cause mortality
A study of 5,303 adults in the National Health and Nutrition Examination Survey (NHANES) cohort assessed the association between phthalate exposure and mortality. Participants provided a urine sample in which the major metabolites of phthalates were measured. Exposure to high-molecular weight phthalates was associated with a significant increase in cardiovascular and all-cause mortality during the duration of the study (2001 to 2010). No significant association was observed for exposure to low-molecular weight total phthalates. Participants who were more exposed to high-molecular weight phthalates (third tertile) had a 48% higher risk of death from any cause than participants who were less exposed (first tertile). Examination of the risk associated with each of the phthalate metabolites revealed an association between an elevated urinary level and a 64% increased risk of cardiovascular mortality for monoethyl phthalate (MEP, a low-molecular weight phthalate). The presence of elevated concentrations of two DEHP (high-molecular weight phthalate) metabolites, MEHHP and MECPP, was associated with a 27% and 32% increased risk of all-cause mortality, respectively, compared to the presence of lower concentrations of these metabolites. A third metabolite of DEHP, MEOHP, was associated with a 74% higher risk of cardiovascular mortality (3rd tertile vs. 1st tertile). Extrapolating the results of their study to the US population aged 55 to 64, the authors estimate that approximately 100,000 deaths/year could be attributed to phthalate exposure, at a societal cost of approximately $39 billion.

Phthalates and where food comes from
One study assessed the phthalate exposure of participants in the NHANES cohort, depending on whether they had a meal the day before outside the home (restaurant, fast food chain, cafeteria) or at home. People who ate out had an average of 35% more phthalates in their urine the next day than people who ate at home, mostly foods purchased from the grocery store. The association between eating out and high urinary phthalate concentration was strongest in adolescents. Among teens, those who reported being heavy consumers of fast food and other foods bought outside the home had up to 55% higher phthalate levels than teens who ate at home. Consumption of certain foods in particular, most notably cheeseburgers and similar sandwiches, was associated with increased cumulative exposure to phthalates, but only when these foods were consumed in cafeterias, fast food outlets, and other restaurants. The study authors find the situation worrisome because almost 2/3 of the population in the United States eats food outside of the home at least once a day.

Phthalates and other plasticizers in fast food
A 2021 study measured the levels of phthalates and another plasticizer in samples of burgers, fries, chicken nuggets, chicken burritos and cheese pizza, as well as in plastic gloves used in fast food restaurants to handle food. Samples came from restaurants of major U.S. chains McDonald’s, Burger King, Pizza Hut, Domino’s, Taco Bell, and Chipotle in the San Antonio, Texas area. DEHT, a new plasticizer used as a replacement for phthalates, was detected in highest amounts in food (median: 2.5 mg/kg) and in gloves (28–37% by weight). DnBP and DEHP phthalates were detected in 81% and 70% of food samples, respectively. DEHT concentrations were particularly high in burritos (6 mg/kg) and in burgers (2.2 mg/kg), and this plasticizer was not present in French fries. Cheese pizza contained the lowest levels of plasticizing chemicals (phthalates or not) among the fast food items analyzed. It should be noted that, unlike phthalates, little data is currently available on the toxicity and health effects of new plasticizers such as DEHT, even though they are increasingly used in industry. The results of this study have implications for equity since the African American population in the United States consumes more fast food than other ethnic groups and is more exposed to chemicals from other sources in the United States in their environment.

Phthalates: endocrine disruptors
In a review of all studies on the impact of phthalate exposure on human health, the authors found strong evidence of unfavourable associations for neurodevelopment, sperm quality, and asthma risk in children, as well as moderate to strong evidence of an association with an anogenital distance abnormality in boys (a marker of exposure to endocrine disruptors). Associations between phthalate exposure and the incidence of type 2 diabetes, endometriosis, low birth weight, low testosterone, ADHD, breast and uterine cancer have also been identified with a moderate level of evidence. Finally, other associations have been identified, but with a lower level of evidence, including premature birth, obesity, autism and hearing loss.

Implications for the public
Standards have been adopted in several countries to limit and, in some cases, prohibit the use of phthalates. For example, the use of certain phthalates in toys for very young children has been banned, as they chew and suck their toys. In cosmetics, the use of DEHP, the most problematic phthalate for health, is banned in Europe and in Canada. According to the European Chemicals Agency (ECHA), the derived no-effect levels (DNEL, or “safe dose”) are 34 µg/kg for DEHP, 8.3 µg/kg for DiBP, 6.7 µg/kg for DnBP, and 500 µg/kg for BBzP. This European agency recommended that the use of these 4 phthalates in the form of mixtures in products be limited to 0.1% (w/w) and that the exception for the use of DEHP in the packaging of medical products be abolished.

A significant problem with these “safe doses” was highlighted for DEHP phthalate since, according to a review of 38 articles, the maximum exposure to DEHP measured in the population is more than 6 times greater than the derived no-effect level (242 vs. 34 µg/kg). In addition, for three other phthalates (DiBP, DnBP and BBzP), the authors reported that adverse health effects were associated with exposure levels much lower than the derived no-effect level established by the ECHA. Among these adverse health effects are increased eczema in children, behavioural changes in children, increased body mass index and waist circumference in women and men, and impacts on the fertility of women and men.

Here are some suggestions for limiting exposure to phthalates:

  • Eat at home as much as possible and limit meals from fast food restaurants to a minimum.
  • In the kitchen, use utensils and containers made of glass, porcelain, stainless steel or wood rather than plastic.
  • Do not heat your meals in the microwave in plastic containers, since the heat increases the release of phthalates in food.
  • Carefully read the list of ingredients for body care products (toothpaste, shampoos, etc.) as manufacturers must indicate the presence of phthalates in their products.
  • For body care, choose natural products that contain few ingredients.
Environmental impacts associated with food production

Environmental impacts associated with food production

OVERVIEW

  • Food production is responsible for about 25% of the greenhouse gases emitted annually, with half of these GHGs coming from animal farming, mainly in the form of methane.
  • The agricultural sector is also an important source of fine particles responsible for air pollution, with the majority of these pollutants coming from ammonia generated by livestock farming.
  • Overall, a reduction in the consumption of animal products, particularly those from cattle farming, is therefore absolutely essential to limit global warming and improve air quality.

The latest report from the Intergovernmental Panel on Climate Change (IPCC) confirms that, if nothing is done, the constant build-up of greenhouse gases (GHG) in the atmosphere will cause temperatures to increase by more than 1.5ºC above pre-industrial levels over the next century, namely the target set by the Paris Agreement to minimize the negative effects of global warming. There is therefore an urgent need to drastically reduce the emission of these gases if we want to prevent the consequences of this warming, already visible today, from becoming out of control and causing an increase in the incidence of extreme climatic events (droughts, heat waves, hurricanes, forest fires), disrupting life on Earth (extinction of species, fall in agricultural yields, increase in infectious diseases, armed conflicts) and increasing the incidence of several diseases linked to excessive heat.

Carbon dioxide and other greenhouse gases
The main greenhouse gas is carbon dioxide (CO2), which now has a concentration of 417 ppm, about twice as much as in pre-industrial times. However, it should be noted that other gases, even if they are present in smaller quantities, also contribute to global warming. These gases, such as methane or certain molecules used for industrial purposes, capture heat in a much greater way than CO2 and therefore have a higher global warming potential (GWP) than CO2. For example, a tonne of methane has a GWP 28 times greater than a tonne of CO2 over a 100-year period, while the GWP of some industrial gases such as sulfur hexafluoride can reach almost 25,000 times that of CO2 (Table 1). In other words, even if many of these gases are present in minute quantities, on the order of a few parts per billion (10-9) or even per trillion (10–12), their emission is several times that of CO2 and therefore significantly contributes to warming.

Table 1. Global warming potential of various greenhouse gases.1 Values are for the year 2018, except for CO2 which is for 2020. Derived from the United States Environmental Protection Agency (EPA).2 Calculated for a 100-year period. From Greenhouse Gas Protocol. *ppm (part per million or 10-6); **ppb (part per billion or 10-9); ***ppt (part per trillion or 10–12).

To calculate this contribution to global greenhouse gas emissions, the method generally used is to convert these emissions into CO2 equivalents (CO2eq) by multiplying their quantity in the atmosphere by their respective GWP. For example, 1 kg of SF6 is equivalent to 23,500 kg (23.5 tonnes) of CO2 (1 kg × 23,500 = 23,500 CO2eq), while it takes 1000 kg of methane to reach an equivalent amount of CO2 (1000 kg × 28 = 28,000 CO2eq). When this method is applied to all gases, it is estimated that 75% of greenhouse gas emissions are in the form of CO2, the remainder coming from methane (17%), nitrous oxide (6%), and various fluorinated gases (2%) (Figure 1).

Figure 1. Distribution of greenhouse gas emissions. Adapted from Ritchie and Roser (2020).


Emissions sources
The use of fossil fuels to support human activities (transport, electricity production, heating, various industrial processes) is the main source of greenhouse gases, accounting for around three quarters of total emissions (Figure 2). This enormous “carbon footprint” implies that the fight against global warming necessarily requires a transition to “cleaner” sources of energy, in particular with regard to transport and electricity production. This is especially true in a country like Canada, where we emit an average of 20 tonnes of CO2eq per person per year, which ranks us, along with the United States and Australia, among the worst producers of GHGs in the world (Quebec, for its part, does better, with about 10 tonnes of CO2eq per person per year).


Figure 2. Contribution of the food sector to the annual production of greenhouse gases. Adapted from Ritchie and Roser (2020).

Another industry that contributes significantly to greenhouse gas emissions, but that we hear much less about, is food production. It is estimated that around 25% of all these gases come from the production and distribution of food, a proportion that rises to 33% when food waste is taken into account. The food sector involved in animal protein production alone is responsible for half of these food-related GHG emissions, mainly due to methane produced by livestock and aquaculture (31%) (see box). Livestock farming also requires large spaces, created in some cases by massive deforestation (in the Amazon, for example), which eliminates huge areas of plants that can sequester COs. Livestock farming also requires large quantities of forage plants and therefore the use of nitrogen fertilizers to accelerate the growth of these plants. The CO2 and nitrous oxide released into the atmosphere during the production of these fertilizers therefore contribute to the GHG generated by livestock.

Where does methane come from?
Methane (CH4) is the end product of the decomposition of organic matter. Methanogenesis is made possible by certain anaerobic microorganisms from the archaea domain (methanogens) which reduce carbon, present in the form of CO2 or certain simple organic acids (acetate, for example), to methane, according to the following reactions:

CO+ 4 H2 → CH4 + 2 H2O

CH3COOH → CH4 + CO2

The methane generated by livestock comes mainly from the fermentation of carbonaceous products inside the digestive system of ruminants. In these animals, the digestion of plant matter generates volatile fatty acids (acetate, propionate, butyrate), which are absorbed by the animal and used as a source of energy, and lead in parallel to the production of methane, about 500 L per day per animal, most of it being released through the mouth of the animal. Globally, livestock is estimated to emit about 3.1 Gt of CO2-eq as methane, which represents almost half of all anthropogenic methane emissions.

Aquaculture is another rapidly expanding form of farming, now accounting for over 60% of the global supply of fish and seafood for human consumption. Although GHG emissions from this sector are still much lower than those associated with livestock, recent measurements nonetheless indicate a sharp increase in its global warming potential, mainly due to an increase in methane production. In these systems, the sediments accumulate food residues used for the growth of fish and seafood as well as the droppings generated by these animals. The transformation of this organic material leads to the production of methane, which can then be diffused into the atmosphere.

Finally, it should be noted that the majority of aquaculture systems are located in Asia, where they are often established in regions previously occupied by mangroves, ecosystems located along the coasts and deltas of tropical regions. The destruction of these mangroves (very often for shrimp farming) is very harmful to global warming, because mangrove forests collectively store around 4 billion tonnes of CO2 and their elimination therefore has a concrete impact on the climate.

A good way to visualize the impact of livestock farming on GHG production is to compare the emissions associated with different foods of animal and plant origin based on the amount of protein in these foods (Figure 3). These comparisons clearly show that products derived from livestock products, beef in particular, represent a much greater source of GHGs than plants. The production of 100 g of beef protein, for example, generates on average 100 times more GHGs than the same amount of protein from nuts or legumes. This is true even for beef produced in the traditional way, i.e., from animals that feed exclusively on grass: these animals grow more slowly and therefore emit methane for a longer period, which cancels out the benefits that could be associated with the sequestration of CO2 by the grass that they eat.

Figure 3. Comparison of GHG levels generated during the production of different protein sources. Based on Poore and Nemecek (2018), as modified by Eikenberry (2018).

These huge differences in GHGs associated with the production of everyday food therefore clearly show that our food choices can have a significant influence on global warming. Since the majority of GHG emissions come from livestock, it is evident that a reduction in the consumption of meat, and animal products as a whole, will have the most positive impact. These benefits can be observed even with a fairly modest reduction in meat intake, as in the Mediterranean diet, or simply by replacing products from ruminants (beef and dairy products) by other sources of animal protein (poultry, pork, fish) (Figure 4). Obviously, a more drastic reduction in meat intake is even more beneficial, whether through the adoption of a flexitarian diet (high intake of plants, but little meat and animal products), vegetarian (no animal products, with the exception of eggs, dairy products and sometimes fish), and vegan (no animal products). This remains true even if the plants consumed come from abroad and sometimes travel long distances, because contrary to popular belief, transport only accounts for a small proportion (less than 10%) of the GHGs associated with a given food.

Figure 4. Potential for mitigation of GHG emissions by different types of diets. Adapted from IPCC (2019).

It is impossible to completely decarbonize food production, especially in a world where there are over 9 billion people to feed daily. On the other hand, there is no doubt that the GHG footprint of food can be significantly reduced by reducing the consumption of products derived from ruminants, such as beef and dairy products. This is extremely important, because the status quo is untenable. According to recent models, even if GHG emissions from fossil fuels ceased immediately, we would still not succeed in reaching the target of a maximum warming of 1.5ºC due to emissions produced by the current food production system.

Another aspect that is often overlooked is how fast and significant this positive impact of a reduction in cattle breeding products can be. Even though methane is a GHG almost 30 times more powerful than CO2, its life in the atmosphere is much shorter, around 10–20 years vs. several thousand years for CO2. Concretely, this means that an immediate drop in methane emissions, for example following a drastic reduction in the consumption of beef and dairy products, can have measurable effects on GHG levels in the following years and therefore represents the fastest and most efficient way to slow global warming.

Pollution from food
In addition to contributing to global GHG emissions, another environmental impact of food production is its contribution to air pollution. This negative impact of the food sector should not be overlooked, because while the influence of global warming caused by GHGs will be felt above all in the medium and longer term, atmospheric pollutants have an immediate effect on health: air pollution is currently the 7th leading cause of premature death worldwide, being directly responsible for around 4 million deaths annually (Figure 5). In some countries, such as the United States, it is estimated that agriculture and livestock are responsible for about 20% of this air pollution-related mortality.

Figure 5. Leading causes of premature mortality worldwide. Note that air pollution is the only risk factor of environmental origin, not related to lifestyle. From GBD 2016 Risk Factors Collaborators (2016).

Fine particles of 2.5 µm and less (PM2.5) are mainly responsible for these negative impacts of air pollution on health. Due to their small size, these particles easily penetrate the lungs to the pulmonary alveoli, where they pass directly to the pulmonary blood vessels and then to all arteries in the body. They then produce an inflammatory reaction and oxidative stress that damage the vascular endothelium, the thin layer of cells that covers the inner walls of the arteries and ensures their proper functioning. The arteries therefore dilate less easily and tend to contract more, which interferes with normal blood circulation. For all these reasons, it is cardiovascular diseases (coronary heart disease and stroke) that represent the main consequence of exposure to fine particles, and alone are responsible for about 80% of all deaths caused by ambient air pollution (Figure 6).

Figure 6. Distribution of premature deaths (in millions) caused by fine particles PM2.5.
Note the predominance of cardiovascular disease as a cause of death linked to air pollution. Adapted from Lelieveld et al. (2015).

Primary and secondary particles
Fine particles can be emitted directly from polluting sources (primary PM2.5) or indirectly, following the combination of several distinct particles present in the atmosphere (secondary PM2.5) (Figure 7). Much of the primary PM2.5 is in the form of carbon soot, produced by the incomplete combustion of fossil fuels (diesel and coal, especially) or biomass (forest fires, for example). Carbon soot is also associated with various organic compounds (polycyclic aromatic hydrocarbons), acids, metals, etc., which contribute to its toxicity after inhalation. These particles can be transported aloft over very long distances and, once deposited, be resuspended in the wind. In urban areas, this resuspension also takes place under the action of road traffic. This turbulence associated with automobile traffic is also responsible for the production of another class of primary PM2.5 called fugitive road dust.

Secondary PM2.5, on the other hand, are formed from precursors such as sulfur dioxide (SO2), nitrogen oxides (NOx), various volatile organic compounds containing carbon (organic carbon) as well as ammonia (NH3). The chemical reactions that govern the interaction between these different volatile substances to form the secondary fine particles are extraordinarily complex, but let us only mention that it is well established that the presence of the ammonium ion (NH4+), derived from ammonia (NH3), neutralizes the negative charge of certain gases and thus promotes their aggregation in the form of fine particles (Figure 7). Consequently, the presence of NH3 in the atmosphere often represents a limiting step in the formation of these secondary fine particles and a reduction in these emissions can therefore have concrete effects on improving air quality.


Figure 7. Schematic representation of the mechanisms of formation of fine particles PM2.5.

It is this important role of ammonia in the formation of secondary fine particles that explains the contribution of the food production sector to air pollution. Agriculture and livestock are in fact responsible for almost all anthropogenic ammonia emissions, a consequence of intensive livestock farming, the spreading of manure and slurry, and the industrial production of nitrogen fertilizers.

An American study clearly illustrates this contribution of agricultural ammonia to the negative impacts of air pollution on health. In this study, the researchers show that of the approximately 18,000 deaths caused annually by pollution derived from the agricultural sector, the vast majority (70%) of these deaths are a consequence of ammonia emissions (and therefore secondary PM2.5), while the emission of primary PM2.5, from plowing, the combustion of agricultural residues, and machinery, is responsible for the rest. Since the vast majority of ammonia emissions come from animal faeces and the use of natural (manure and slurry) or synthetic fertilizers to grow food for these animals, it is not surprising that the production of food from livestock is the main cause of deaths attributable to pollution from agricultural sources (Figure 8).

Figure 8. Distribution of deaths caused annually by PM2.5 from the agricultural sector in the United States. Note that 70% of the mortality is attributable to livestock products, mainly due to the ammonia generated by the animals as well as by the spreading of manure, slurry and synthetic fertilizers for the cultivation of fodder plants (corn, soybeans). From Domingo et al. (2021).

When we compare the impact of different foods for the same quantity of product, we immediately see that the production of red meat is particularly damaging, being responsible for at least 5 times more deaths than that of poultry, 10 times more than that of nuts and seeds, and at least 50 times more than that of other plants such as fruits and vegetables (Figure 9).

Figure 9. Comparison of PM2.5-related mortality by food types. From Domingo et al. (2021).

In short, whether in terms of reducing GHG emissions or health problems associated with atmospheric pollution, all the studies unequivocally show that a reduction in environmental damage caused by food production necessarily involves a reduction in the consumption of products of animal origin, in particular those from cattle farming. A change that is all the more profitable as the reduction in the intake of food of animal origin, combined with an increase in the consumption of plants, is beneficial for health and could prevent about 11 million premature deaths annually, a decrease of 20%.

The impact of forest fires on human health

The impact of forest fires on human health

OVERVIEW

  • Wildfires will be increasingly frequent given climate change that is leading to higher temperatures and drought in many parts of the world.
  • Smoke from forest fires produces fine and ultrafine particles that can travel up to 1,000 kilometres and affect the health of people from afar.
  • In the short term, smoke from wildfires is mainly harmful to respiratory health. Some populations are more at risk of suffering the consequences.
  • The increase in forest fires may in turn contribute to climate disruption.

 

From British Columbia to the island of Evia, wildfires are increasingly part of the global landscape. The health impacts of these blazes on global health are unequivocal. Here is an overview of a natural phenomenon exacerbated by climate change.

The recent report of the IPCC, the Intergovernmental Panel on Climate Change, highlights that forest fires are likely to be more frequent and severe given the acceleration of climate change.1 Higher temperatures favour the development of lightning, which is the main natural cause of wildfires. A climate predicted to be drier and windier will promote combustion and the spread of forest fires.2 The fire season will therefore last longer. By 2039, the frequency of fires could increase over 37.8% of the planet with a rise of just 1.2 °C in global temperature. With an increase of 3.5 °C, 61.9% of the world territory will be affected by more frequent fires by 2100.3 In the most pessimistic climate scenario where greenhouse gas emissions continue to rise, this risk will affect up to 74% of the world’s land surface by the end of the century. The United States, Canada, Mediterranean countries, China and Australia will be particularly affected.4

In Canada, it is estimated that more than 8,000 fires occur each year. On average, more than 2.1 million hectares are destroyed annually, equivalent to the area of Victoria Island.5 In all the provinces, weather conditions will be increasingly conducive to wildfires. The areas burned could thus double by 2100.6

The smoke from wildfires is made up of carbon monoxide, carbon dioxide, nitrogen oxides, and other organic compounds. These vary according to several factors, such as the type of vegetation and the temperature of the fire.7 Fires also produce fine particles (diameter ≤ 2.5 μm or PM2.5) and ultrafine particles (diameter ≤ 0.1 μm or PM0.1) that can travel up to 1,000 km.2 It is mainly these particles that are harmful to the health of populations living at a distance from fire outbreaks. Fine particles produced by wildfires may also contain more oxidative and pro-inflammatory compounds than urban air pollution caused by burning fossil fuels.8 One study suggests that fine particles from wildfires may be 10 times more harmful to human health than those produced by other sources.9

Impact on human health

Population near forest fires
Populations near fires and first responders are at risk of direct injury from burns, heat, and direct smoke inhalation. Smoke can also irritate the eyes, cause corneal abrasions, reduce visibility, and increase the risk of traffic accidents in areas near the fires.10

Respiratory health
For local or remote populations, fine and ultrafine particles enter the respiratory tract and cause inflammation to the lungs. Exposure to fine particles mainly causes respiratory symptoms, such as coughing or difficulty breathing.7

Many exposed individuals will not have any symptoms, but some are more likely to develop them. The extent of exposure to smoke and the presence of vulnerability factors may modulate the severity of the clinical presentation, as shown in Figure 1.

Figure 1. Clinical and subclinical impact of fine particles from wildfires. From Cascio (2018).11

Patients with asthma or chronic obstructive pulmonary disease may experience more exacerbations of their respiratory symptoms, use more medications to control them, and seek more health care services.121314 People aged 65 and over, those working outdoors, and those residing in disadvantaged neighbourhoods are also more vulnerable to fine particles from fires.15 Children are also more susceptible to the harmful effects of smoke. A less well-developed immune system and a higher basal respiratory rate in children could explain this vulnerability.2

Cardiovascular health
Are the fine particles produced specifically by forest fires harmful to cardiovascular health? The answer remains to be clarified. While some studies show a significant risk of cardiovascular disease associated with exposure, others do not.1416

Among these, a study analyzing 2.5 million hospitalizations in areas 200 km from wildfires in the United States suggests that the risk of cardiovascular disease may be comparable to that of urban air pollution.17

Another study conducted on the 2015 California wildfires shows an association between exposure to smoke and increased emergency room visits related to cardiovascular diseases, such as myocardial infarction, ischemic heart disease, heart failure, hypertension, and arrhythmias. Adults 65 years of age and older were particularly affected. An association between smoke density and cerebrovascular events, such as stroke, has also been noted by researchers.18

Australian studies have also shown an association between exposure to fine particles from wildfires and the risk of cardiac arrest in the community.1920

Of note, short-term exposure (less than 3 hours) to smoke produced by burning wood has the potential to increase central arterial stiffness, heart rate and decrease heart rate variability. In other words, wood smoke could have harmful hemodynamic effects on the cardiovascular system.21

In short, fine particles from fires are added to those generated by global air pollution, well known to worsen the incidence of cardiovascular disease.

Mortality
Exposure to smoke from forest fires is associated with an increased risk of mortality from non-specific and non-accidental causes.2 In Canada, from 2013 to 2018, 620 to 2,700 premature deaths were reported to have been caused by smoke from forest fires.22 Current data do not allow us to establish a clear link between exposure to fine particles from forest fire smoke and an increase in mortality from a specific cause, such as respiratory or cardiac.

However, it should be noted that short-term exposure to fine particles caused by global air pollution is associated with an increased risk of mortality.23 Even short-term exposure to fine particles could increase the risk of myocardial infarction mortality.24 In other words, smoke from wildfires could be a risk factor for cardiovascular mortality, but this has yet to be clarified.

Other effects on physical health
Some studies suggest that pregnant women exposed to fine particles from forest fires may be at greater risk of giving birth prematurely or having a low birth weight baby. However, the data remain limited and should be interpreted with caution.2

In addition, one study found a marked increase in the number of influenza cases a few months after intense forest fires in the Montana region (USA). This could suggest a certain vulnerability to respiratory infections following exposure to smoke.25 The fine particles produced by fires could alter the function of macrophages, cells of the immune system, reducing the body’s ability to effectively defend itself against respiratory tract infections.26 In this sense, some researchers are currently evaluating the impact of air pollution from forest fires on the transmission and severity of COVID-19 cases.272829

Overall, more studies are needed to better understand the medium- and long-term impact of wildfire smoke on human health.

Mental health
Wildfires can be devastating for the communities living nearby. Emergency evacuations and the loss of one’s physical and social environment are intense stressors that can have an impact on mental health, particularly in children and adolescents.30 People directly exposed to wildfires are at greater risk of major depression, post-traumatic stress disorder, and anxiety disorders.10 Access to psychological support services is therefore essential for populations strongly affected by forest fires.

Socio-economic impacts
Wildfires are also associated with greater use of medical resources. There are more medical consultations in emergency rooms, family medicine clinics and hospitalizations.31 In Canada, the annual health costs associated with fine particles from forest fires are estimated at between $410 million and $1.8 billion for short-term exposure. From $4.3 billion to $19 billion are attributable to chronic exposure.22 This adds to many societal costs, such as those associated with rebuilding infrastructure, contamination of drinking water by smoke ash, and loss of income.11

Environmental health
Although exacerbated by human pollution, wildland fires themselves contribute to climate change. Combined with the continued emission of greenhouse gases from human activities, the loss of vegetation reduces the absorption of carbon dioxide and thus contributes to the increase in the temperature of the earth. Forest fires could also contribute to the melting of permafrost and thus promote the emission of methane,2 a gas whose potential for warming the atmosphere is 25 times greater than carbon dioxide.32

What to do about forest fires?

Learn about air quality
In Canada, the Air Quality Health Index provides information about air quality across the country33 and the FireWork forecasting system helps predict the movement of smoke from forest fires.34 The Canadian government’s WeatherCAN application is also a weather forecasting tool accessible to the population.35 Local authorities are also responsible for issuing air quality warnings and health recommendations.

Reduce exposure to air pollution
Figure 2 summarizes the main measures to be taken to reduce the impact of wildfire smoke on health. In order to limit exposure to fine particles following a forest fire, recommendations may vary depending on the location. The net effectiveness of these interventions still needs to be clarified, as they are based on a limited number of small-scale studies.36 It is advisable to avoid outdoor activities, including physical exercise, when the atmospheric level of fine particles is too high.15

In order to reduce the infiltration of outdoor air into buildings, it is useful to close doors and windows if the heat is not too overwhelming inside. High levels of fine particles in the atmosphere can be associated with intense heat waves. If the temperature inside is too high, the heat can be harmful to health, especially in the elderly or those with chronic diseases. Setting the heating, ventilation and air conditioning systems to recirculation mode and limiting the use of the kitchen hood are also recommended measures to reduce air intake.37

Air purifiers with HEPA (high efficient particulate air) filters effectively reduce the level of fine particles and are recommended by the Government of Canada. However, these are not able to remove some polluting gases from the air. In addition, air purifiers can be expensive and therefore less accessible to everyone.2

As for wearing a mask, the surgical type is not recommended, since it does not protect against fine particles. N95 masks offer better protection, but they require an individual fit test, can give a false sense of security, and are not suitable for children. The use of these masks is recommended for workers exposed to smoke from fires.38 Finally, the creation of community smoke-free spaces is also a measure that can be implemented by local authorities when the level of air pollution increases.39

Figure 2. Key actions individuals can take to reduce exposure to wildfire smoke and its health risks. From Rongbin et al. (2020)2


Preventing climate change
Globally, the main goal to reduce forest fires and their health consequences would be to limit the global temperature increase to 1.5 °C instead of the 2° C targeted by the Paris Agreement. This limited increase would prevent more than 50% of the predicted forest fires if the global temperature rises by 2° C.4

The IPCC report highlights that even the 2° C target will be exceeded without massive and imminent interventions. Concerted government actions are therefore more than necessary to substantially reduce anthropogenic greenhouse gas emissions.

Conclusion In sum, the air pollution emitted by forest fires is associated with an increase in morbidity and mortality. Some health effects remain to be elucidated. These increasingly frequent fires reflect the impact of climate change on human health. In the short and long term, interventions and prevention measures to protect the population will be necessary in order to mitigate the social, economic and environmental consequences of these climatic upheavals.  

 

References

(1) IPCC, 2021: Summary for Policymakers. In: Climate Change 2021: The Physical Science Basis. Contribution of Working Group I to the Sixth Assessment Report of the Intergovernmental Panel on Climate Change . Cambridge University Press.

(2) Rongbin X et al. Wildfires, global climate change, and human health. N. Engl. J. Med. 2020; 383(22): 2173-2181.

(3) Hoegh-Guldberg OD et al. (2018). Impacts of 1.5oC Global Warming on Natural and Human Systems. In: Global Warming of 1.5°C. An IPCC Special Report on the impacts of global warming of 1.5°C above pre-industrial levels and related global greenhouse gas emission pathways, in the context of strengthening the global response to the threat of climate change, sustainable development, and efforts to eradicate poverty.

(4)  Sun Q et al. Global heat stress on health, wildfires, and agricultural crops under different levels of climate warming. Environment Int. 2019; 128:125-136.

(5) Gouvernement du Canada  (2019). Base nationale de données sur les feux de forêt du Canada (BNDFFC).

(6) Gouvernement du Canada (2020). Changement climatique et feux.

(7) Benmarhnia T et al. (2013). Les impacts sanitaires liés aux incendies de forêt. Institut national de santé publique du Québec, N° de publication : 1679.

(8) Wegesser TC et al. California wildfires of 2008: coarse and fine particulate matter toxicity. Environ. Health Perspect. 2009; 117(6): 893–897.

(9) Aguilera RC et al. Wildfire smoke impacts respiratory health more than fine particles from other sources: observational evidence from Southern California. Nature Commun. 2021; 12: 1493.

(10) Finlay SE et al. Health impacts of wildfires. PLoS Curr. 2012; 4: e4f959951cce2c.

(11) Cascio WE. Wildland fire smoke and human health. Sci.Total Environ. 2018; 624: 586-595.

(12) Johnston FH et al.  Vegetation fires, particulate air pollution and asthma: A panel study in the Australian monsoon tropics. Int. J. Environ. Health Res. 2006; 16(6): 391-404.

(13) Caamano-Isorna F et al. Respiratory and mental health effects of wildfires: an ecological study in Galician municipalities (north-west Spain). Environ. Health 2011; 10: 48.

(14) Black C et al. Wildfire smoke exposure and human health: Significant gaps in research for a growing public health issue. Environ. Toxicol. Pharmacol. 2017; 55: 186-195.

(15) Rice MB et al. Respiratory impacts of wildland fire smoke: future challenges and policy opportunities. Ann. Am. Thorac. Soc. 2021; 18(6): 921-930.

(16) Reid CE et al. Critical review of health impacts of wildfire smoke exposure. Environ. Health Perspect. 2016; 124(9): 1334–1343.

(17) DeFlorio-Barker S et al. Cardiopulmonary effects of fine particulate matter exposure among older adults, during wildfire and non-wildfire periods, in the United States 2008–2010. Environ. Health Perspect. 2019; 127(3): 37006.

(18) Wettstein ZS et al.  Cardiovascular and cerebrovascular emergency department visits associated with wildfire smoke exposure in California in 2015. J. Am. Heart Assoc. 2018; 7(8): e007492.

(19) Haikerwal A et al. Impact of fine particulate matter (PM2.5) exposure during wildfires on cardiovascular health outcomes. J. Am. Heart Assoc. 2015; 4(7): e001653.

(20) Dennekamp M et al. Forest fire smoke exposures and out-of-Hospital cardiac arrests in Melbourne, Australia: a case-Crossover study. Environ. Health Perspect. 2015; 123(10): 954-624.

(21) Unosson J et al. Exposure to wood smoke increases arterial stiffness and decreases heart rate variability in humans. Part. Fibre Toxicol. 2013; 10: 20.

(22) Matz CJ et al. Health impact analysis of PM2.5 from wildfire smoke in Canada (2013–2015, 2017–2018). Sci. Total Environ. 2020; 725: 138506.

(23) Di Q et al. Association of short-term exposure to air pollution with mortality in older adults. JAMA 2017; 318(24): 2446–2456.

(24) Liu Y et al.  Short-term exposure to ambient air pollution and mortality from myocardial infarction. J. Am. Coll. Cardiol. 2021; 77(3): 271-281.

(25) Landguth EL et al. The delayed effect of wildfire season particulate matter on subsequent influenza season in a mountain west region of the USA. Environ Int. 2020; 139: 105668.

(26) Migliaccio CT et al.  (2013). Adverse effects of wood smoke PM(2.5) exposure on macrophage functions. Inhal Toxicol. 2013; 25(2): 67–76.

(27) Henderson SB. The COVID-19 pandemic and wildfire smoke: potentially concomitant disasters. Am. J. Public Health 2020; 110(8): 1140-1142.

(28) Kiser D et al. SARS-CoV-2 test positivity rate in Reno, Nevada : association with PM2.5 during the 2020 wildfire smoke events in the western United States. J. Expo. Sci. Environ. Epidemiol., publié le 13 juillet 2021.

(29) Zhou X et al. Excess of COVID-19 cases and deaths due to fine particulate matter exposure during the 2020 wildfires in the United States. Sci Adv. 2021; 7(33): eabi8789.

(30) Brown MRG et al.  After the Fort McMurray wildfire there are significant increases in mental health symptoms in grade 7-12 students compared to controls. BMC Psychiatry 2019 ; 19: 18.

(31) Moore D et al.  Population health effects of air quality changes due to forest fires in British Columbia in 2003: estimates from physician-visit billing data. Can. J. Public Health 2006; 97(2): 105-108.

(32) IPCC, 2007: Climate Change 2007: The Physical Science Basis. Contribution of Working Group I to the Fourth Assessment Report of the Intergovernmental Panel on Climate Change . Cambridge University Press, Cambridge, United Kingdom and New York, NY, USA, 996 pp.

(33) Gouvernement du Canada. Cote Air Santé.

(34) Gouvernement du Canada. Système de prévision de la fumée des feux de forêt pour le Canada (FireWork).

(35) Government of Canada. WeatherCAN.

(36) Laumbach RJ (2019). Clearing the air on personal interventions to reduce exposure to wildfire smoke. Ann. Am. Thorac. Soc. 2019; 16(7): 815-818.

(37) Gouvernement du Canada. Lignes directrices relatives aux espaces antifumée pendant les épisodes de fumée de feux de forêt.

(38) Environmental Health Services, BC Centre for Disease Control. (2014) Guidance for BC Public Health Decision Makers During Wildfire Smoke Events.

(39) Wheeler AJ et al.  Can public spaces effectively be used as cleaner indoor air shelters during extreme smoke events? Int. J. Environ. Res. Public Health 2021; 18(8): 4085.