Daily hospital admissions for asthma and upper respiratory infections, air pollutants, outdoor pollen, and temperature in New York City, from 1999 to 2009.

<p>Daily hospital admissions for asthma and upper respiratory infections, air pollutants, outdoor pollen, and temperature in New York City, from 1999 to 2009.</p

Relative risks^a of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m³ increase in PM_2.5 concentrations in New York City, from 1999 to 2009.

<p>Relative risks<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180522#t002fn002" target="_blank">^a</a> of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m³ increase in PM_2.5 concentrations in New York City, from 1999 to 2009.</p

Confounding effects of hospital admissions for Upper Respiratory Infections (URI) on the associations between asthma hospital admissions in school-age children and ozone (top) and PM_2.5 (bottom).

<p>URI is included in the main model as log-transformed daily counts of all-age URI HA. Squares are point estimates for relative risks of asthma hospital admissions associated with increases in air pollutants. The dashed lines represent ±10% changes in the point estimates from the main model.</p

Relative risks^a of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m3 increase in PM_2.5 concentrations at Lag 0–1 in New York City, stratified by socioeconomic status, during warm seasons from 2002 to 2006.

<p>Relative risks<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0180522#t003fn002" target="_blank">^a</a> of hospital admissions for asthma per 10 ppb increase in ozone concentrations or per 10 μg/m3 increase in PM_2.5 concentrations at Lag 0–1 in New York City, stratified by socioeconomic status, during warm seasons from 2002 to 2006.</p

Confounding effects of outdoor pollen on the associations between asthma hospital admissions in school-age children and ozone (top) and PM_2.5 (bottom).

<p>Squares are point estimates for relative risks of asthma hospital admissions associated with increases in air pollutants. The dashed lines represent ±10% changes in the point estimates from the main model.</p

Quantitative cancer risk assessment for occupational exposures to asphalt fumes during built-up roofing asphalt (BURA) operations

<div><p></p><p>The International Agency for Research on Cancer qualitatively characterized occupational exposure to oxidized bitumen emissions during roofing as probably carcinogenic to humans (Group 2A). We examine chemistry, exposure, epidemiology and animal toxicity data to explore quantitative risks for roofing workers applying built-up roofing asphalt (BURA). Epidemiology studies do not consistently report elevated risks, and generally do not have sufficient exposure information or adequately control for confounders, precluding their use for dose–response analysis. Dermal carcinogenicity bioassays using mice report increased tumor incidence with single high doses. In order to quantify potential cancer risks, we develop time-to-tumor model methods [consistent with US Environmental Protection Agency (EPA) dose–response analysis and mixtures guidelines] using the dose–time–response shape of concurrent exposures to benzo[<i>a</i>]pyrene (B[<i>a</i>]P) as concurrent controls (which had several exposure levels) to infer presumed parallel dose–time–response curves for BURA-fume condensate. We compare EPA relative potency factor approaches, based on observed relative potency of BURA to B[<i>a</i>]P in similar experiments, and direct observation of the inferred BURA dose–time–response (scaled to humans) as means for characterizing a dermal unit risk factor. We apply similar approaches to limited data on asphalt-fume inhalation and respiratory cancers in rats. We also develop a method for adjusting potency estimates for asphalts that vary in composition using measured fluorescence. Overall, the various methods indicate that cancer risks to roofers from both dermal and inhalation exposure to BURA are within a range typically deemed acceptable within regulatory frameworks. The approaches developed may be useful in assessing carcinogenic potency of other complex mixtures of polycyclic aromatic compounds.</p></div

Ozone exposure and systemic biomarkers: Evaluation of evidence for adverse cardiovascular health impacts

<div><p></p><p>The US Environmental Protection Agency (EPA) recently concluded that there is likely to be a causal relationship between short-term (< 30 days) ozone exposure and cardiovascular (CV) effects; however, biological mechanisms to link transient effects with chronic cardiovascular disease (CVD) have not been established. Some studies assessed changes in circulating levels of biomarkers associated with inflammation, oxidative stress, coagulation, vasoreactivity, lipidology, and glucose metabolism after ozone exposure to elucidate a biological mechanism. We conducted a weight-of-evidence (WoE) analysis to determine if there is evidence supporting an association between changes in these biomarkers and short-term ozone exposure that would indicate a biological mechanism for CVD below the ozone National Ambient Air Quality Standard (NAAQS) of 75 parts per billion (ppb). Epidemiology findings were mixed for all biomarker categories, with only a few studies reporting statistically significant changes and with no consistency in the direction of the reported effects. Controlled human exposure studies of 2 to 5 hours conducted at ozone concentrations above 75 ppb reported small elevations in biomarkers for inflammation and oxidative stress that were of uncertain clinical relevance. Experimental animal studies reported more consistent results among certain biomarkers, although these were also conducted at ozone exposures well above 75 ppb and provided limited information on ozone exposure-response relationships. Overall, the current WoE does not provide a convincing case for a causal relationship between short-term ozone exposure below the NAAQS and adverse changes in levels of biomarkers within and across categories, but, because of study limitations, they cannot not provide definitive evidence of a lack of causation.</p></div