The sentiment that woodsmoke, being a natural substance, must be benign to humans is still sometimes heard. It is now well established, however, that wood-burning stoves and fireplaces as well as wildland and agricultural fires emit significant quantities of known health-damaging pollutants, including several carcinogenic compounds. Two of the principal gaseous pollutants in woodsmoke, CO and NOx, add to the atmospheric levels of these regulated gases emitted by other combustion sources. Health impacts of exposures to these gases and some of the other woodsmoke constituents (e.g., benzene) are well characterized in thousands of publications. As these gases are indistinguishable no matter where they come from, there is no urgent need to examine their particular health implications in woodsmoke. With this as the backdrop, this review approaches the issue of why woodsmoke may be a special case requiring separate health evaluation through two questions. The first question we address is whether woodsmoke should be regulated and/or managed separately, even though some of its separate constituents are already regulated in many jurisdictions. The second question we address is whether woodsmoke particles pose different levels of risk than other ambient particles of similar size. To address these two key questions, we examine several topics: the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related

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Woodsmoke Health Effects: A Review

Polycyclic aromatic hydrocarbons (PAHs), of which benzo[a]pyrene is the most commonly studied and measured, are formed by the incomplete combustion of organic matter. They are widely distributed in the environment and human exposure to them is unavoidable. A number of them, such as benzo[a]pyrene, are carcinogenic and mutagenic, and they are widely believed to make a substantial contribution to the overall burden of cancer in humans. Their presence in the environment is reflected in their presence at detectable levels in many types of uncooked food. In addition, cooking processes can generate PAHs in food. PAHs can also be formed during the curing and processing of raw food prior to cooking. Several studies have been carried out to determine the levels of exposure to PAHs from representative human diets, and the proportion of the overall burden of environmental exposure to PAHs that is attributable to the diet. In most cases, it is concluded that diet is the major source of human exposure to PAHs. The major dietary sources of PAHs are cereals and vegetables, rather than meat, except where there is high consumption of meat cooked over an open flame. More recently, biomonitoring procedures have been developed to assess human exposure to PAHs and these have also indicated that diet is a major source of exposure. Exposure to nitro-PAHs through food consumption appears to be very low.

Polycyclic aromatic hydrocarbons in the diet.

Polycyclic aromatic hydrocarbons (PAHs) are a family of toxicants that are ubiquitous in the environment. These contaminants generate considerable interest, because some of them are highly carcinogenic in laboratory animals and have been implicated in breast, lung, and colon cancers in humans. These chemicals commonly enter the human body through inhalation of cigarette smoke or consumption of contaminated food. Of these two pathways, dietary intake of PAHs constitutes a major source of exposure in humans. Although many reviews and books on PAHs have been published, factors affecting the accumulation of PAHs in the diet, their absorption following ingestion, and strategies to assess risk from exposure to these hydrocarbons following ingestion have received much less attention. This review, therefore, focuses on concentrations of PAHs in widely consumed dietary ingredients along with gastrointestinal absorption rates in humans. Metabolism and bioavailability of PAHs in animal models and the processes, which influence the disposition of these chemicals, are discussed. The utilitarian value of structure and metabolism in predicting PAH toxicity and carcinogenesis is also emphasized. Finally, based on intake, disposition, and tumorigenesis data, the exposure risk to PAHs from diet, and contaminated soil is presented. This information is expected to provide a framework for refinements in risk assessment of PAHs from a multimedia exposure perspective.

https://journals.sagepub.com/doi/pdf/10.1080/10915810490517063

Bioavailability and risk assessment of orally ingested polycyclic aromatic hydrocarbons.

Diets containing substantial amounts of red or preserved meats may increase the risk of various cancers, including colorectal cancer. This association may be due to a combination of factors such as the content of fat, protein, iron, and/or meat preparation (e.g., cooking or preserving methods). Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Humans can be exposed to NOCs by exogenous routes (from processed meats in particular) and by endogenous routes. Endogenous exposure to NOCs is dose-dependently related to the amount of red meat in the diet. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). To investigate the role of these compounds, we have created separate databases for HCAs and PAHs, which we have used in conjunction with a validated meat-cooking food frequency questionnaire. The role of meat type, cooking methods, doneness levels, and meat-cooking mutagens has been examined in both case-control studies and prospective cohort studies, with mixed results. Here, we review the current epidemiologic knowledge of meat-related mutagens, and evaluate the types of studies that may be required in the future to clarify the association between meat consumption and colorectal cancer.

Meat‐related mutagens/carcinogens in the etiology of colorectal cancer

Evidence shows that fetuses and infants are more affected than adults by a variety of environmental toxicants because of differential exposure, physiologic immaturity, and a longer lifetime over which disease initiated in early life can develop. In this article we review data on the effects of in utero exposure to common environmental contaminants, including polycyclic aromatic hydrocarbons (PAH), particulate matter and environmental tobacco smoke (ETS). We then summarize results from our molecular epidemiologic study to assess risks from in utero exposures to ambient air pollution and ETS. This research study, conducted in Poland, used biomarkers to measure the internal and bioeffective dose of toxicants and individual susceptibility factors. The study included 160 mothers and 160 newborns. Ambient air pollution was significantly associated (p= 0.05) with the amount of PAH bound to DNA (PAH-DNA adducts) in both maternal and infant cord white blood cells (WBC). Newborns with elevated PAH-DNA adducts (greater than the median) had significantly decreased birth weight (p= 0.05), birth length (p= 0.02), and head circumference (p= 0.0005) compared to the newborns with lower adducts (n= 135). Maternal and infant cotinine levels were increased by active and passive cigarette smoke exposure of the mother (p= 0.01). An inverse correlation was seen between newborn plasma cotinine (nanograms per milliliter) and birth weight (p= 0.0001) and length (p= 0.003). Adducts were elevated in placental tissue and WBC of newborns who were heterozygous or homozygous for the cytochrome P4501A1 MspI restriction fragment length polymorphism (RFLP) compared to newborns without the RFLP. Levels of PAH-DNA and cotinine were higher in newborns than mothers. These results document that there is significant transplacental transfer of PAH and ETS constituents from mother to fetus; that PAH-DNA adduct levels in maternal and newborn WBC were increased with environmental exposure to PAH from ambient pollution; and that the fetus is more sensitive to genetic damage than the mother. The study also provided the first molecular evidence that transplacental PAH exposure to the fetus is compromising fetal development. If confirmed, these findings could have significant public health implications since a number of studies have found that reduction of head circumference at birth correlates with lower intelligence quotient as well as poorer cognitive functioning and school performance in childhood.

Molecular epidemiologic research on the effects of environmental pollutants on the fetus.

The effect of ingesting charcoal-broiled (CB) beef on polycyclic aromatic hydrocarbon (PAH)-DNA adduct levels in nucleated peripheral white blood cells (WBCs) was examined in four healthy, non-smoking males who consumed an average of 280 g CB beef daily for 7 days. PAH-DNA adducts were quantitated by enzyme-linked immunosorbent assay. During the week of CB beef consumption, two individuals exhibited a 3- to 6-fold increase in PAH-DNA adducts above baseline levels observed during the month prior to CB beef consumption. In contrast, PAH-DNA adduct levels in the two other subjects did not increase. Thus, dietary sources of PAH can contribute to the PAH-DNA adduct load in peripheral WBCs in some individuals.

Formation of polycyclic aromatic hydrocarbon-DNA adducts in peripheral white blood cells during consumption of charcoal-broiled beef

We studied cross-seasonal changes in pulmonary function and respiratory symptoms in 52 wildland firefighters in Northern California. The mean cross-seasonal change in forced expiratory volume in 1 second (FEV1) was -1.2% (95% confidence interval [CI] -0.5%, -2.0%) with a corresponding mean change in forced expiratory volume (FVC) of -0.3% (95% CI 0.4%, -1.0%). Decreases in FEV1 and FVC were most strongly associated with hours of recent fire-fighting activity (P = .002 and .01, respectively). When the study group was divided into three categories based on recent fire-fighting activity, firefighters in the high activity category (mean +/- SE, 73 +/- 7 hours of fire-fighting in previous week) had a -2.9% (130 mL) change in FEV1 and a -1.9% (102 mL) change in forced vital capacity (FVC). There was a significant cross-seasonal increase in most respiratory symptoms evaluated. Several symptoms (eye irritation, nose irritation, and wheezing) were associated with recent fire-fighting. These findings suggest that wildland firefighters experience a small cross-seasonal decline in pulmonary function and an increase in several respiratory symptoms. Research is under way to identify the fire conditions and specific components of exposure that produce pulmonary irritants, and to examine the potential reversibility of acute pulmonary change.

Pulmonary function and respiratory symptoms in wildland firefighters.

Previous investigations suggest that dietary sources of polycyclic aromatic hydrocarbons (PAHs) contribute to the PAH-DNA adduct load in peripheral white blood cells (WBCs). In the current study, we measured PAH-DNA adducts by enzyme-linked immunosorbent assay in WBCs obtained from 47 California wildland (forest) firefighters at two time points (early and late) during an active forest fire season. PAH-DNA adduct levels were not associated with recent firefighting activity, but were positively associated with frequency of charbroiled food consumption in the previous 2 weeks. In addition, adduct levels declined with time since last ingestion of charbroiled food. These studies indicate that recent consumption of charbroiled food contributes to the PAH-DNA adduct load in peripheral WBCs.

Association of PAH-DNA adducts in peripheral white blood cells with dietary exposure to polyaromatic hydrocarbons

Determinations of baseline sister-chromatid exchanges (SCE) have been used extensively as indicators of previous mutagen exposure in both animals and humans. Hypersensitivity to mutagen-induced SCE levels has also been studied in a variation on the basic technique as an indication of previous mutagen exposure in a stressed or provocative test system. The genotoxicity of the alkylating anti-cancer drugs including cyclophosphamide (CP) has been examined previously by determining baseline SCEs in peripheral blood lymphocytes from treated cancer patients. This study examined the in-vivo genotoxic effects of CP therapy by comparing baseline and phosphoramide mustard (PM)-induced SCEs in therapeutically (in-vivo) treated cancer patients with SCE levels in newly diagnosed, but not treated patients. Therapeutically treated patients showed statistically higher baseline SCE frequencies than untreated control patients with a mean SCE/cell of 6.95 vs. 5.25, p less than 0.016. When net SCE values (induced minus baseline) were determined in PM-exposed cells in-vitro both at low dose (0.1 microgram/ml PM) and high dose (0.25 microgram/ml PM) however, the difference was not significant between therapeutically treated and untreated control patients. The return to control SCE levels as a function of time since last therapeutic treatment was also evaluated and no difference was found between the rate of decline of PM-induced SCEs and baseline SCE levels over time.

Baseline and phosphoramide mustard-induced sister-chromatid exchanges in cancer patients treated with cyclophosphamide

The occupational illnesses most frequently reported to the Occupational Safety and Health Administration (OSHA) are "disorders associated with repeated trauma," a category including noise-induced hearing loss and illnesses caused by ergonomic exposure. In response, OSHA has begun "rule-making" for a standard to control ergonomic exposures. This paper defines ergonomic illness as any diagnosis of gradual onset for which ergonomic exposure increases relative risk. The "Red Meat Guidelines," the model for OSHA's proposed "Ergonomic Safety and Health Program standard," are critically reviewed in terms of basic clinical and epidemiologic concepts. The OSHA 200 log is a cohort study which reaches its entire target population. The use of selected case definitions with the OSHA 200 log is recommended as a powerful, comparable, and cost-effective epidemiologic basis for ergonomic regulation.

J.A. Hansen

Papers

Formation of polycyclic aromatic hydrocarbon-DNA adducts in peripheral white blood cells during consumption of charcoal-broiled beef

Pulmonary function and respiratory symptoms in wildland firefighters.

Association of PAH-DNA adducts in peripheral white blood cells with dietary exposure to polyaromatic hydrocarbons

Baseline and phosphoramide mustard-induced sister-chromatid exchanges in cancer patients treated with cyclophosphamide

OSHA regulation of ergonomic health.