Potential for Electric Vehicle Adoption to Mitigate Extreme Air Quality Events in China.

Electric vehicle (EV) adoption promises potential air pollutant and greenhouse gas (GHG) reduction co-benefits. As such, China has aggressively incentivized EV adoption, however much remains unknown with regard to EVs' mitigation potential, including optimal vehicle type prioritization, power generation contingencies, effects of Clean Air regulations, and the ability of EVs to reduce acute impacts of extreme air quality events. Here, we present a suite of scenarios with a chemistry transport model that assess the potential co-benefits of EVs during an extreme winter air quality event. We find that regardless of power generation source, heavy-duty vehicle (HDV) electrification consistently improves air quality in terms of NO2 and fine particulate matter (PM2.5), potentially avoiding 562 deaths due to acute pollutant exposure during the infamous January 2013 pollution episode (~1% of total premature mortality). However, HDV electrification does not reduce GHG emissions without enhanced emission-free electricity generation. In contrast, due to differing emission profiles, light-duty vehicle (LDV) electrification in China consistently reduces GHG emissions (~2 Mt CO2), but results in fewer air quality and human health improvements (145 avoided deaths). The calculated economic impacts for human health endpoints and CO2 reductions for LDV electrification are nearly double those of HDV electrification in present-day (155M vs. 87M US$), but are within ~25% when enhanced emission-free generation is used to power them. Overall, we find only a modest benefit for EVs to ameliorate severe wintertime pollution events, and that continued emission reductions in the power generation sector will have the greatest human health and economic benefits.

Public Health and Climate Benefits and Trade-Offs of U.S. Vehicle Electrification.

Vehicle electrification is a common climate change mitigation strategy, with policymakers invoking co-beneficial reductions in carbon dioxide (CO2) and air pollutant emissions. However, while previous studies of U.S. electric vehicle (EV) adoption consistently predict CO2 mitigation benefits, air quality outcomes are equivocal and depend on policies assessed and experimental parameters. We analyze climate and health co-benefits and trade-offs of six U.S. EV adoption scenarios: 25% or 75% replacement of conventional internal combustion engine vehicles, each under three different EV-charging energy generation scenarios. We transfer emissions from tailpipe to power generation plant, simulate interactions of atmospheric chemistry and meteorology using the GFDL-AM4 chemistry climate model, and assess health consequences and uncertainties using the U.S. Environmental Protection Agency Benefits Mapping Analysis Program Community Edition (BenMAP-CE). We find that 25% U.S. EV adoption, with added energy demand sourced from the present-day electric grid, annually results in a ~242 M ton reduction in CO2 emissions, 437 deaths avoided due to PM2.5 reductions (95% CI: 295, 578), and 98 deaths avoided due to lesser ozone formation (95% CI: 33, 162). Despite some regions experiencing adverse health outcomes, ~$16.8B in damages avoided are predicted. Peak CO2 reductions and health benefits occur with 75% EV adoption and increased emission-free energy sources (~$70B in damages avoided). When charging-electricity from aggressive EV adoption is combustion-only, adverse health outcomes increase substantially, highlighting the importance of low-to-zero emission power generation for greater realization of health co-benefits. Our results provide a more nuanced understanding of the transportation sector's climate change mitigation-health impact relationship.

Emergency Department Visits and Ambient Temperature: Evaluating the Connection and Projecting Future Outcomes.

The U.S. Global Climate Change Research Program has identified climate change as a growing public health threat. We investigated the potential effects of changes in ambient daily maximum temperature on hyperthermia and cardiovascular emergency department (ED) visits using records for patients age 64 and younger from a private insurance database for the May-September period for 2005-2012. We found a strong positive relationship between daily maximum temperatures and ED visits for hyperthermia but not for cardiovascular conditions. Using the fitted relationship from 136 metropolitan areas, we calculated the number and rate of hyperthermia ED visits for climates representative of year 1995 (baseline period), as well as years 2050 and 2090 (future periods), for two climate change scenarios based on outcomes from five global climate models. Without considering potential adaptation or population growth and movement, we calculate that climate change alone will result in an additional 21,000-28,000 hyperthermia ED visits for May to September, with associated treatment costs between $6 million and $52 million (2015 U.S. dollars) by 2050; this increases to approximately 28,000-65,000 additional hyperthermia ED visits with treatment costs between $9 million and $118 million (2015 U.S. dollars) by 2090. The range in projected additional hyperthermia visits reflects the difference between alternative climate scenarios, and the additional range in valuation reflects different assumptions about per-case valuation.

Development of a heat vulnerability index for New York State.

OBJECTIVES: The frequency and intensity of extreme heat events are increasing in New York State (NYS) and have been linked with increased heat-related morbidity and mortality. But these effects are not uniform across the state and can vary across large regions due to regional sociodemographic and environmental factors which impact an individual's response or adaptive capacity to heat and in turn contribute to vulnerability among certain populations. We developed a heat vulnerability index (HVI) to identify heat-vulnerable populations and regions in NYS. STUDY DESIGN: Census tract level environmental and sociodemographic heat-vulnerability variables were used to develop the HVI to identify heat-vulnerable populations and areas. METHODS: Variables were identified from a comprehensive literature review and climate-health research in NYS. We obtained data from 2010 US Census Bureau and 2011 National Land Cover Database. We used principal component analysis to reduce correlated variables to fewer uncorrelated components, and then calculated the cumulative HVI for each census tract by summing up the scores across the components. The HVI was then mapped across NYS (excluding New York City) to display spatial vulnerability. The prevalence rates of heat stress were compared across HVI score categories. RESULTS: Thirteen variables were reduced to four meaningful components representing 1) social/language vulnerability; 2) socioeconomic vulnerability; 3) environmental/urban vulnerability; and 4) elderly/ social isolation. Vulnerability to heat varied spatially in NYS with the HVI showing that metropolitan areas were most vulnerable, with language barriers and socioeconomic disadvantage contributing to the most vulnerability. Reliability of the HVI was supported by preliminary results where higher rates of heat stress were collocated in the regions with the highest HVI. CONCLUSIONS: The NYS HVI showed spatial variability in heat vulnerability across the state. Mapping the HVI allows quick identification of regions in NYS that could benefit from targeted interventions. The HVI will be used as a planning tool to help allocate appropriate adaptation measures like cooling centers and issue heat alerts to mitigate effects of heat in vulnerable areas.

Quantitative measurement of airborne cockroach allergen in New York City apartments.

UNLABELLED: We designed and tested a sampling and analysis system for quantitative measurement of airborne cockroach allergen with sufficient sensitivity for residential exposure assessment. Integrated 1-week airborne particle samples were collected at 10-15 LPM in 19 New York City apartments in which an asthmatic child who was allergic to cockroach allergen resided. Four simultaneous air samples were collected in each home: at heights of 0.3 and 1 m in the child's bedroom and in the kitchen. Extracts of air samples were analyzed by ELISA for the cockroach allergen Bla g2, modified by amplifying the colorimetric signal generated via use of AMPLI-Q detection system (DAKO Corporation, Carpinteria, CA, USA). Settled dust samples were quantified by conventional ELISA. Of the homes where cockroach allergen was detected in settled dust, Bla g2 also was detected in 87% and 93% of air samples in the bedroom and kitchen, respectively. Airborne Bla g2 levels were highly correlated within and between the bedroom and kitchen locations (P < 0.001). Expressed as picogram per cubic meter, the room average geometric mean for Bla g2 concentrations was 1.9 pg/m³ (95% CI 0.63, 4.57) and 3.8 pg/m³ (95% CI 1.35, 9.25) in bedrooms and kitchens, respectively. This method offers an attractive supplement to settled dust sampling for cockroach allergen exposure health studies. PRACTICAL IMPLICATIONS: Until now, cockroach allergen exposures have usually been assessed by collection and analysis of settled dust, on the assumption that airborne cockroach allergen cannot be reliably measured. In this study, a sensitive and quantitative method for measuring indoor airborne exposures to cockroach allergens involving a 7-day integrated total suspended particulate (TSP) sample collected at approximately 10-15 l/min was developed. Investigators are now empowered with an alternative exposure assessment method to supplement their studies and the understanding of allergen aerodynamics in the homes of children with asthma. We report airborne cockroach allergen in apartments, suggesting an ongoing burden of inhalation exposure.

A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures.

Inner-city minority populations are high-risk groups for adverse birth outcomes and also more likely to be exposed to environmental contaminants, including environmental tobacco smoke (ETS), benzo[a]pyrene B[a]P, other ambient polycyclic aromatic hydrocarbons (global PAHs), and residential pesticides. The Columbia Center for Children's Environmental Health (CCCEH) is conducting a prospective cohort study of 700 northern Manhattan pregnant women and newborns to examine the effects of prenatal exposure to these common toxicants on fetal growth, early neurodevelopment, and respiratory health. This paper summarizes results of three published studies demonstrating the effects of prenatal ETS, PAH, and pesticides on birth outcomes and/or neurocognitive development [Perera FP, Rauh V, Whyatt RM, Tsai WY, Bernert JT, Tu YH, et al. Molecular evidence of an interaction between prenatal environment exposures on birth outcomes in a multiethnic population. Environ Health Perspect 2004;12:630-62; Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, et al. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol 2004;26:373-85; Whyatt RM, Rauh V, Barr DB, Camann DE, Andrews HF, Garfinkel R, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environ Health Perspect, in press]. To evaluate the effects of prenatal exposure to ETS, PAHs, and pesticides, researchers analyzed questionnaire data, cord blood plasma (including biomarkers of ETS and pesticide exposure), and B[a]P-DNA adducts (a molecular dosimeter of PAHs). Self-reported ETS was associated with decreased head circumference (P = 0.04), and there was a significant interaction between ETS and adducts such that combined exposure had a significant multiplicative effect on birth weight (P = 0.04) and head circumference (P = 0.01) after adjusting for confounders. A second analysis examined the neurotoxic effects of prenatal ETS exposure and postpartum material hardship (unmet basic needs in the areas of food, housing, and clothing) on 2-year cognitive development. Both exposures depressed cognitive development (P < 0.05), and there was a significant interaction such that children with exposure to both ETS and material hardship exhibited the greatest cognitive deficit (7.1 points). A third analysis found that cord chlorpyrifos, and a combined measure of cord chlorpyrifos, diazinon, and propoxur-metabolite, were inversely associated with birth weight and/or length (P < 0.05). These results underscore the importance of policies that reduce exposure to ETS, air pollution, and pesticides with potentially adverse effects on fetal growth and child neurodevelopment.

Biomarkers in assessing residential insecticide exposures during pregnancy and effects on fetal growth.

The Columbia Center for Children's Environmental Health is using a combination of environmental and biologic measures to evaluate the effects of prenatal insecticide exposures among urban minorities in New York City. Of the 571 women enrolled, 85% report using some form of pest control during pregnancy and 46% report using exterminators, can sprays, and/or pest bombs. Chlorpyrifos, diazinon, and propoxur were detected in 99.7-100% of 48-h personal air samples collected from the mothers during pregnancy (n = 394) and in 39-70% of blood samples collected from the mothers (n = 326) and/or newborns (n = 341) at delivery. Maternal and newborn blood levels are similar and highly correlated (r = 0.4-08, P < 0.001). Levels of insecticides in blood samples and/or personal air samples decreased significantly following the 2000-2001 U.S. Environmental Protection Agency's regulatory actions to phase out residential use of chlorpyrifos and diazinon. Among infants born prior to 1/1/01, birth weight decreased by 67.3 g (95% confidence interval (CI) -116.6 to -17.8, P = 0.008) and birth length decreased by 0.43 centimeters (95% CI, -0.73 to -0.14, P = 0.004) for each unit increase in log-transformed cord plasma chlorpyrifos levels. Combined measures of (ln)cord plasma chlorpyrifos and diazinon (adjusted for relative potency) were also inversely associated with birth weight and length (P 0.8). Results support recent regulatory action to phase out residential uses of these insecticides.

Prenatal exposure, maternal sensitization, and sensitization in utero to indoor allergens in an inner-city cohort.

Primary sensitization to antigens may occur prenatally. We hypothesized that high prenatal exposure to indoor antigens increases the risk for sensitization in newborns in New York City populations with increased risk for asthma. We also investigated whether maternal sensitization is required for in utero sensitization to occur. One hundred sixty-seven pregnant African American or Dominican women residing in northern Manhattan were recruited and antigen was measured from home dust. After delivery, newborn cord and maternal blood were assayed for IgE and mononuclear cell proliferation and cytokine production in response to antigen. Cockroach, mouse, but not dust mite antigens, were commonly elevated in the kitchens and pregnant mothers' beds. Increased mononuclear cell proliferation occurred in 54% of newborns in response to cockroach, 25% in response to dust mite Dermatophagoides pteronyssinus, 40% in response to dust mite D. farinae, and 34% in response to mouse protein extracts. Antigen-induced mononuclear cell proliferation occurred in cord blood even in the absence of antigen-induced mononuclear cell proliferation in the mother. Proliferation in response to antigens did not correlate with IgE levels, but proliferation in response to dust mite extracts correlated with interluekin-5 (IL-5) production in cord blood. These results suggest that (1) high prenatal exposures to cockroach and mouse antigens are prevalent; (2) in utero sensitization to multiple indoor antigens is common, occurs to a different degree than maternal sensitization, and may involve IL-5 upregulation.

Respiratory effects of seasonal exposures to ozone and particles.

Whereas human respiratory effects of brief ozone exposures are well documented, much less is known about the human health effects of mid- to long-term exposures. The authors' objective in this study was to determine whether lung function or respiratory symptom changes would occur over the course of a summer season among healthy young adults working outdoors in the presence of ozone. The authors studied 72 sophomore cadets from the U.S. Military Academy at West Point, New York, 21 of whom attended special summer training in Fort Dix, New Jersey, an area characterized by elevated ozone levels; the remaining cadets attended training in areas with moderate ozone levels (i.e., Fort Benning, Georgia; Fort Leonard Wood, Missouri; and Fort Sill, Oklahoma). The authors hypothesized that adverse respiratory outcomes, if any, would be more pronounced in the group exposed to higher ozone levels. Spirometry was performed and respiratory symptoms were assessed-both before and after the summer-in a clinic at West Point. Time spent outdoors during summer training averaged 11 hr/d. Both mean and peak ozone levels were higher at Fort Dix than at the three remaining sites. Regional levels of sulfur dioxide and particulate matter less than 10 microm in aerodynamic diameter were relatively low during the study. However, all cadets reported frequent exposure to dust, exhaust, and smoke in the course of their training. Averaged across all subjects, there was a statistically significant drop in forced expiratory volume in 1 sec of 44 ml (p = .035) over the summer. There were also significant increases in reports of cough, chest tightness, and sore throat at the follow-up clinic visit. A larger mean forced expiratory volume in 1 sec decline was observed at Fort Dix, where ozone exposures were the highest. The results of this study demonstrated a seasonal decline in respiratory function among healthy young adults working outdoors in the presence of ozone and particulate matter.

Air pollution and daily hospital admissions in metropolitan Los Angeles.

We used daily time-series analysis to evaluate associations between ambient carbon monoxide, nitrogen dioxide, particulate matter [less than and equal to] 10 microm in aerodynamic diameter (PM(10)), or ozone concentrations, and hospital admissions for cardiopulmonary illnesses in metropolitan Los Angeles during 1992-1995. We performed Poisson regressions for the entire patient population and for subgroups defined by season, region, or personal characteristics, allowing for effects of temporal variation, weather, and autocorrelation. CO showed the most consistently significant (p<0.05) relationships to cardiovascular admissions. A wintertime 25th-75th percentile increase in CO (1.1-2.2 ppm) predicted an increase of 4% in cardiovascular admissions. NO(2), and, to a lesser extent, PM(10) tracked CO and showed similar associations with cardiovascular disease, but O(3) was negatively or nonsignificantly associated. No significant demographic differences were found, although increased cardiovascular effects were suggested in diabetics, in whites and blacks (relative to Hispanics and Asians), and in persons older than 65 years of age. Pulmonary disease admissions associated more with NO(2) and PM(10) than with CO. Pulmonary effects were generally smaller than cardiovascular effects and were more sensitive to the choice of model. We conclude that in Los Angeles, atmospheric stagnation with high primary (CO/NO(2)/PM(10)) pollution, most common in autumn/winter, increases the risk of hospitalization for cardiopulmonary illness. Summer photochemical pollution (high O(3)) apparently presents less risk.

Airborne concentrations of PM(2.5) and diesel exhaust particles on Harlem sidewalks: a community-based pilot study.

Residents of the dense urban core neighborhoods of New York City (NYC) have expressed increasing concern about the potential human health impacts of diesel vehicle emissions. We measured concentrations of particulate matter [less than/equal to] 2.5 micro in aerodynamic diameter (PM(2.5)) and diesel exhaust particles (DEP) on sidewalks in Harlem, NYC, and tested whether spatial variations in concentrations were related to local diesel traffic density. Eight-hour (1000-1800 hr) air samples for PM(2.5 )and elemental carbon (EC) were collected for 5 days in July 1996 on sidewalks adjacent to four geographically distinct Harlem intersections. Samples were taken using portable monitors worn by study staff. Simultaneous traffic counts for diesel trucks, buses, cars, and pedestrians were carried out at each intersection on [Greater/equal to] 2 of the 5 sampling days. Eight-hour diesel vehicle counts ranged from 61 to 2,467 across the four sites. Mean concentrations of PM(2.5) exhibited only modest site-to-site variation (37-47 microg/m(3)), reflecting the importance of broader regional sources of PM(2.5). In contrast, EC concentrations varied 4-fold across sites (from 1.5 to 6 microg/m(3)), and were associated with bus and truck counts on adjacent streets and, at one site, with the presence of a bus depot. A high correlation (r = 0.95) was observed between EC concentrations measured analytically and a blackness measurement based on PM(2.5) filter reflectance, suggesting the utility of the latter as a surrogate measure of DEP in future community-based studies. These results show that local diesel sources in Harlem create spatial variations in sidewalk concentrations of DEP. The study also demonstrates the feasibility of a new paradigm for community-based research involving full and active partnership between academic scientists and community-based organizations.

Long-term residence in areas of high ozone: associations with respiratory health in a nationwide sample of nonsmoking young adults [dsee comments].

Few studies have examined the respiratory effects of multiyear ozone exposures in human populations. We examined associations between current respiratory health status and long-term ozone exposure histories in 520 Yale College (New Haven, CT) students who never smoked. Questionnaires addressed current respiratory symptoms, respiratory disease history, residential history, and other factors. The symptoms of cough, phlegm, wheeze apart from colds, and a composite respiratory symptom index (RSI) were selected as outcome measures. Forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV(1)), forced expiratory flow rate between 25 and 75% of FVC (FEF(25-75)), and forced expiratory flow rate at 75% of FVC (FEF(75)) were obtained by forced expiration into spirometers. Ozone exposure was treated as a dichotomous variable, where subjects were assigned to the high-exposure group if they lived for 4 or more years in a U.S. county with 10-year average summer-season daily 1-hr maximum ozone levels [greater/equal to] 80 ppb. Lung function and respiratory symptoms were analyzed by multiple linear and logistic regression on ozone exposure, controlling for covariates. Lung function was lower in the group with high ozone exposures: differences were statistically significant for FEV(1) [-3.1%; 95% confidence interval (CI), -0.2 to -5.9%] and FEF(25-75) (-8.1%; CI, -2.3 to -13.9%), and nearly so for FEF(75) (-6.7%; CI, 1.4 to -14.8). Gender-specific analyses revealed stronger associations for males than for females. The symptoms of chronic phlegm, wheeze apart from colds, and RSI were increased in the ozone-exposed group, with odds ratios of 1.79 (CI, 0.83-3.82), 1.97 (CI, 1.06-3.66), and 2.00 (CI, 1.15-3.46), respectively. We conclude that living for 4 or more years in regions of the country with high levels of ozone and related copollutants is associated with diminished lung function and more frequent reports of respiratory symptoms.

Diesel exhaust exposure among adolescents in Harlem: a community-driven study.

OBJECTIVES: This study sought individual-level data on diesel exhaust exposure and lung function among adolescents in Harlem as part of a community-driven research agenda. METHODS: High school students administered in-person surveys to seventh grade students to ascertain information on demographics, asthma history, and self-reported and maternal smoking. Urine samples were assayed for 1-hydroxypyrene (1-HP), a marker of diesel exhaust exposure, and cotinine, a marker of tobacco smoke exposure. Computer-assisted spirometry was used to measure lung function. RESULTS: Three quarters (76%) of the participating students had detectable levels of 1-HP. Three students (13%) had an FEF25-75 of less than or equal to 80% of their predicted measurements, and 4 students (17%) had results between 80% and 90% of the predicted value, all of which are suggestive of possible lung impairment. CONCLUSIONS: These data suggest that most adolescents in Harlem are exposed to detectable levels of diesel exhaust, a known exacerbator and possible cause of chronic lung disorders such as asthma. Community-driven research initiatives are important for empowering communities to make needed changes to improve their environments and health.

Methods development for epidemiologic investigations of the health effects of prolonged ozone exposure. Part III. An approach to retrospective estimation of lifetime ozone exposure using a questionnaire and ambient monitoring data (U.S. sites).

Methods are needed for retrospective estimation of long-term ozone exposures in epidemiologic studies. The overall objective of this study was to evaluate whether data from available U.S. ozone monitoring sites are useful for estimating lifetime ozone exposures of young adults (for example, college students). Several aspects of this question were evaluated. First, we applied and (compared several spatial interpolation methods to a set of long-term average ozone data from all U.S. monitoring sites in operation from 1981 through 1990. Interpolation methods included simple and weighted averages, linear regression, and, in an exploratory way, kriging. The comparison of methods was carried out for five different metrics of ozone concentration: the daily one-hour maximum (MAX1) and eight-hour maximum (MAX8), the average ozone concentrations between 10 a.m. and 6 p.m. (MID8) and between 10 a.m. and 10 p.m. (MID12), and the sum of all hourly ozone concentrations greater than or equal to 60 parts per billion (ppb) (SUM06). We also tested whether interpolations were improved by modeling the influence of covariates such as population density, elevation, and weather on ozone concentrations. We analyzed the reliability of a set of newly developed questions about past activity levels among a group of 52 freshmen students at Yale University. This was done by analyzing the agreement between answers to the same questionnaire administered two times, one month apart (test and retest), to the same students. Finally, we combined the interpolation models with residential history information obtained by questionnaire to derive long-term ozone exposure estimates for a group of 200 Yale freshmen. Results of our study showed that the density of available monitoring sites appears to be adequate for estimating spatial patterns of long-term average ambient ozone concentrations. A simple regression-based interpolation on the three nearest sites produced consistently good results. Including covariates in the interpolation models did not substantially improve the estimates. The largest estimation errors occurred for areas where ozone concentrations were highest. The newly developed activity history questions exhibited fair to moderate reliability, The results of this work imply that reasonably precise estimates of long-term ambient ozone concentrations for use in large-scale epidemiologic studies can be achieved by interpolating ozone concentrations between available U.S. monitoring sites. This study did not address the issues of whether and how retrospective data on factors that modify exposure or dose (e.g., indoor/outdoor penetration of ozone and time outdoors) can be used to derive estimates of long-term personal ozone exposures and contribute to the assessment of received dose.

Biomarkers of lung inflammation in recreational joggers exposed to ozone.

Humans exhibit an acute inflammatory response in the lungs after controlled laboratory exposure to ozone. The present study was designed to test whether biomarkers of inflammation are detectable in humans exposed to ozone and associated copollutants under natural conditions outdoors. Bronchoscopy with bronchoalveolar lavage (BAL) was carried out on 19 normal volunteer joggers from Governors Island, NY, who exercised in the afternoon during the 1992 summer (S1) season. Fifteen subjects were retested during the following, low ozone, winter season (W). The BAL protocol involved an initial instillation of 20 ml saline followed by four sequential 50-ml saline washes carried out in both the right middle lobe and the lingula. The eight 50-ml samples were pooled as the 'alveolar' sample. Analyses performed on the alveolar lavage samples included cell differentials, release of IL-8, TNF-alpha, and reactive oxygen species (ROS) by pooled cells, and levels of IL-8, protein, LDH, fibronectin, alpha1-antitrypsin (alpha1-AT), complement fragment 3a (C3a), and prostaglandin E2 (PGE2) in lavage fluids. Release of ROS by stimulated BAL cells was lower in S1 than in W (p = 0.03). In contrast, LDH levels in BAL fluids were 2-fold higher in S1 than in W (p = 0.02), as were IL-8 (p = 0.12) and PGE2 (p = 0.06). These results suggest a possible ongoing inflammatory response in the lungs of recreational joggers exposed to ozone and associated copollutants during the summer months.

The effects of ambient ozone on lung function in children: a reanalysis of six summer camp studies.

Studies of children attending summer camps often have observed relationships between daily outdoor ozone (O3) concentrations and decreased lung function that are qualitatively similar to results seen in human chamber studies. The former studies, focusing on the pulmonary effects of O3 and associated pollutants on children under natural conditions of exposure, are potentially of great importance to understanding the public health impact of ambient O3. However, a thorough assessment of the results of these studies has been hampered by differences in the analysis and reporting of data across the various studies. We obtained data sets from six summer camp studies carried out by three separate investigative groups, including two New Jersey studies performed by New York University, two studies in Ontario carried out by Health and Welfare Canada, and two studies in southern California. The data consisted of sequential, daily measurements of forced expiratory volume in 1 sec (FEV1), peak expiratory flow rate (PEFR), and 1-hr O3 concentration in the hour preceding lung function measurements for each child. We analyzed the relationships between lung function and O3 using linear regression models that fit subject-specific intercepts and a single, pooled O3 slope. These models were fit for each of the six studies separately and for all studies combined. All of the study-specific slopes of FEV1 on O3 were negative (i.e., increased O3 associated with decreased FEV1); five of six were statistically significant. Analysis of the combined six-study data set yielded a slope of -0.50 ml FEV1/ppb O3 (p<0.0001). Addition of time-trend variables to the combined-data analysis diminished, but did not eliminate, the FEV1-O3 relationship. Study-specific slopes for PEFR on O3 were more variable. Combined over studies, no significant relationship was observed between PEFR and O3. However, this negative finding appeared to be partially confounded by time trends in PEFR. The results of this reanalysis provide strong evidence that children exposed to O3 under natural conditions experience decreases in FEV1 of the kind demonstrated in laboratory studies, and raise concern that other acute respiratory effects observed in those studies (e.g., pulmonary inflammation) may also occur in young people exposed to ambient O3.

Interaction of nickel with mutagens in the induction of sister chromatid exchanges in human lymphocytes.

In this study, individual treatments of human lymphocytes with Ni(II) [0.5-25 microM], Cr(VI) [0.65-1.30 microM], UV-light or X-rays induced SCEs in a dose-dependent fashion, and combined treatments of Ni(II) with Cr(VI), UV-light or X-rays interacted antagonistically. Nickel, at environmentally relevant exposure levels, can have the effect in complex mixtures of reducing an otherwise positive SCE response and could lead to underestimating human exposures to certain classes of chemicals or radiation. Furthermore, our data indicate that antagonism may occur when human lymphocytes are exposed simultaneously to Ni(II) and Cr(VI), suggesting an explanation for epidemiological studies reporting conflicting results for cytogenetic effects in lymphocytes of workers exposed to chromium and nickel.

Ni(II) induced changes in cell cycle duration and sister-chromatid exchanges in cultured human lymphocytes.

Investigations from our laboratory and others have shown that Ni(II) treatments of cultured human lymphocytes produced a relatively small but significant increase in SCE frequency. Based on the known effects of Ni(II) on DNA replication, we evaluated whether Ni(II) produced a cell cycle delay in lymphocytes. Human lymphocytes of three normal subjects were exposed to 5, 10, and 25 microM of NiSO4 in culture medium and scored for the percent of metaphases in the first (M1), second (M2), and third (M3) cell cycle for harvest times spaced every 4 h from 36 to 72 h after culture initiation. Cell cycle duration was studied using Tice's BISACK method with certain modifications. All three doses of NiSO4 caused a delay of nearly 1.5 h in the initiation of cell division, but only 25 microM NiSO4 caused a lengthening in the cell cycle time of nearly 4 h for completion of the first cycle. Only at the highest dose of Ni(II) was there a significant increase in the SCE frequency compared to the control. When the proliferation rate index (PRI) was examined, the effect of 5 or 10 microM Ni(II) was negligible while the 25 microM concentration caused a suppression in the proliferation rate. The effect of Ni(II) on the cell cycle was much more pronounced than on the PRI. A significant increase in SCE frequency was observed only for the concentration of Ni(II) that caused a pronounced cell cycle delay, a result that is consistent with prior studies showing higher SCE responses for chemical treatments that lengthen the cell cycle.

Effects of nickel ions on polymerase activity and fidelity during DNA replication in vitro.

Nickel is a genotoxic carcinogen. However, the mechanisms of nickel-induced genotoxicity are not well understood. We have investigated the effects of Ni2+ ions on DNA polymerase activity and the fidelity of DNA replication in vitro. The effect of Ni2+ on different DNA polymerases is quite variable. The amount of enzyme inhibition and degree of alteration in replication fidelity induced by Ni2+ are dependent both on the polymerase and its associated 3'-5' exonuclease activity. Some polymerases, such as E. coli DNA polymerase I, AMV reverse transcriptase and human DNA polymerase alpha, can utilize Ni2+ as a weak substitute for Mg2+ during DNA replication. Other polymerases are very sensitive to inhibition by Ni2+ and the IC50 can vary by an order of magnitude. T4 polymerase is relatively insensitive to inhibition by Ni2+, although the sensitivity is enhanced in the absence of added Mg2+, and Ni preferentially inhibits the 3'-5' exonuclease function of T7 DNA polymerase. The fidelity and processivity of DNA polymerases may be either increased or decreased by Ni ions in a polymerase dependent manner. The inhibition DNA polymerase activity and altered replication fidelity may contribute significantly to Ni-induced mutagenesis and genotoxicity in vivo.

A multi-year study of air pollution and respiratory hospital admissions in three New York State metropolitan areas: results for 1988 and 1989 summers.

As part of a multi-year study of air pollution and respiratory hospital admissions in the Buffalo, Albany, and New York City, New York, metropolitan areas, filter samples were collected daily at suburban air monitoring sites and analyzed for their content of particulate phase aerosol strong acidity (i.e., hydrogen ion, H+) and sulfate (SO4 = ). In addition, daily hospital admissions for respiratory causes, other community air pollutant measurements (e.g., ozone, O3), and meteorological data (e.g., temperature) were also obtained for these metropolitan areas. The summer months (June-August) were selected for analysis because that is when the highest H+ (and O3) are usually experienced at these sites, and because these months are rarely complicated by other major influences (e.g., high pollen counts). Thus, any pollution-admissions relationships were expected to be most clearly discernible in this season. Prior to the health effects analysis, the summer admissions and environmental data were first detrended to eliminate long-wave autocorrelations, and day-of-week effects were removed via regression. Cross-correlations of the filtered 1988 and 1989 admissions and environmental data revealed strong associations between elevated summer haze pollution (i.e., H+, SO4 =, and O3) and increased total respiratory and asthma admissions on the same day and/or on subsequent days in Buffalo and New York City, especially during the summer of 1988 (when pollution levels were more extreme). Regression analyses indicated that the pollution-admissions associations remained significant (p < 0.05) even after the simultaneous inclusion of lagged daily maximum temperature. Mean effects calculations for these cities indicated that summertime haze can play a significant role in the occurrence of respiratory admissions in that season: accounting for an average 6 to 24% of 1988 Buffalo and NYC asthma admissions (depending on the pollutant index employed). O3 consistently had the highest mean effects estimates. Relative risk (RR) calculations indicated that the risk of admission for asthma was increased by a factor of 1.19 to 1.43 in these cities on maximum 1988 summertime pollution days, with H+ consistently having the highest RR estimates. These results are consistent with the hypothesis that ambient acid aerosol peaks (e.g., H+ > or = 100 nmol/m3) can potentiate the respiratory disease effects of O3. Associations were weaker in the less urbanized Albany metropolitan area and in the New York City (NYC) suburbs, even though the NYC suburban O3 exposures were similar to (and the H+ concentrations may even be somewhat higher than) those in the center city.(ABSTRACT TRUNCATED AT 400 WORDS)