Academic journal article Environmental Health Perspectives

Ranking Cancer Risks of Organic Hazardous Air Pollutants in the United States

Academic journal article Environmental Health Perspectives

Ranking Cancer Risks of Organic Hazardous Air Pollutants in the United States

Article excerpt

The U.S. Clean Air Act designates hazardous air pollutants (HAPs) as those that "may reasonably be anticipated to be carcinogenic, mutagenic" (Clean Air Act Amendments 1990), and exhibit other adverse health effects. Effective reduction of exposures to HAPs requires determining the compounds, exposure pathways, and sources that contribute the most to human health risk.

Many prior risk assessments for HAPs have been limited by either including only indoor or outdoor concentrations or by examining only a small subset of carcinogenic HAPs. The U.S. Environmental Protection Agency (EPA) assessed the nationwide risk from outdoor concentrations of most of the HAPs. Based on the Assessment System for Population Exposure Nationwide (ASPEN) model (U.S. EPA 2000), the U.S. EPA found that almost half of total estimated lifetime cancer cases from HAPs could be attributed to volatile organic compounds (VOCs), with another 40% from polycyclic aromatic compounds (PAHs) (Woodruff et al. 2000). The median cancer risk was 17 cases of every 100,000 people. An updated assessment finds a median risk of 4 in 100,000 (U.S. EPA 2006a), accounting for changes in emissions estimates and lower cancer potency values for some of the larger contributors to risk (particularly 1,3-butadiene and formaldehyde). However, outdoor exposures account for only a portion of risk for many compounds.

In two older studies using indoor concentrations from homes and offices, one by Tancrede et al. (1987) and another by McCann et al. (1986), calculated cancer potency factors with data from animal and human studies. Tancrede et al. found annual mean risks from indoor air to be about 1 in 10,000 to 1 in 100,000, and McCann et al.'s risks are about an order of magnitude higher (McCann et al. 1986; Tancrede et al. 1987). Concentrations of many of these compounds, however, have changed since these studies were completed.

Personal exposure measurements from the Total Exposure Assessment Methodology (TEAM) studies provided estimates of individual cancer risks from benzene ranging from 1 in 10,000 for nonsmokers to 7 in 10,000 for smokers (Wallace 1991a). More recently, Payne-Sturges et al. (2004) found risks from personal exposure over three times higher than those calculated using the ASPEN modeled outdoor concentrations. Sax et al. (2006) also found risks from personal exposures of inner-city teenagers to be on the order of 1 in 10,000. Despite these studies, there has not been a broad analysis of cancer risk integrating total personal exposure to a wide range of organic HAPs in multiple microenvironments and across different exposure pathways. Also, two potentially high-risk classes of HAPs have not been included in previous personal exposure risk assessments--the dioxins and the PAHs.

Exposure to semivolatile HAPs, such as dioxins/furans and PAHs, can also come from noninhalation pathways, especially food ingestion (Butler et al. 1993; Ramesh et al. 2004; U.S. EPA 2003). Although these compounds are primarily released to the air, some fraction is bound to particulate matter and then deposited onto vegetation or water bodies where they build up in the food chain. Multimedia sampling has been done previously (Butler et al. 1993; Chuang et al. 1999), but only for a specific compound or class of compounds, and the risks of multipathway exposures have not been analyzed or compared across compound groups.

To gain a wider perspective on population risks from organic HAPs, we estimated the cancer risks in the United States by using calculated total personal exposure. We restricted ourselves to organic compounds that were responsible in aggregate for >87% of the risk according to Woodruff et al. (2000), along with several others with known indoor sources or for which ingestion is a main route of exposure. We chose first to model baseline exposures, defined as those not including specifically known and consistent high exposure scenarios. …

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