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In a cohort of 6338 California Seventh-day Adventists, we previously observed for males associations between long-term concentrations of particulate matter (PM) with an aerodynamic diameter less than 10 microm (PM10) and 15-year mortality due to all natural causes (ANC) and lung cancer (LC) listed as underlying causes of death and due to nonmalignant respiratory disease listed as either the underlying or a contributing (CRC) cause of death. The purpose of this analysis was to determine whether these outcomes were more strongly associated with the fine (PM2.5) or the coarse (PM2.5-10) fractions of PM10. For participants who lived near an airport (n=3769), daily PM2.5 concentrations were estimated from airport visibility, and on a monthly basis, PM2.5-10 concentrations were calculated as the differences between PM10 and PM2.5. Associations between ANC, CRC, and LC mortality (1977-1992) and mean PM10, PM2.5, and PM2.5-10 concentrations at study baseline (1973-1977) were assessed using Cox proportional hazards models. Magnitudes of the PM10 associations for the males of this subgroup were similar to those for the males in the entire cohort although not statistically significant due to the smaller numbers. In single-pollutant models, for an interquartile range (IQR) increase in PM10 (29.5 microg/m3), the rate ratios (RRs) and 95% confidence intervals (CI) were 1.15 (0.94, 1.41) for ANC, 1.48 (0.93, 2.34) for CRC, and 1.84 (0.59, 5.67) for LC. For an IQR increase in PM2.5 (24.3 microg/m3), corresponding RRs (95% CI) were 1.22 (0.95, 1.58), 1.64 (0.93, 2.90), and 2.23 (0.56, 8.94), and for an IQR increase in PM2.5-10 (9.7 microg/m3), corresponding RRs (95% CI) were 1.05 (0.92, 1.20), 1.19 (0.88, 1.62), and 1.25 (0.63, 2.49), respectively. When both PM25 and PM2.5-10 were entered into the same model, the PM2.5 estimates remained stable while those of PM2.5-10 decreased. We concluded that previously observed associations of long-term ambient PM10 concentration with mortality for males were best explained by a relationship of mortality with the fine fraction of PM10 rather than with the coarse fraction of PM10.

Long-term ambient concentrations of inhalable particles less than 10 microm in diameter (PM10) (1973- 1992) and other air pollutants-total suspended sulfates, sulfur dioxide, ozone (O3), and nitrogen dioxide-were related to 1977-1992 mortality in a cohort of 6,338 nonsmoking California Seventh-day Adventists. In both sexes, PM10 showed a strong association with mortality for any mention of nonmalignant respiratory disease on the death certificate, adjusting for a wide range of potentially confounding factors, including occupational and indoor sources of air pollutants. The adjusted relative risk (RR) for this cause of death as associated with an interquartile range (IQR) difference of 43 d/yr when PM10 exceeded 100 microg/m3 was 1.18 (95% confidence interval [CI]: 1.02, 1.36). In males, PM10 showed a strong association with lung cancer deaths-RR for an IQR was 2.38 (95% CI: 1.42, 3.97). Ozone showed an even stronger association with lung cancer mortality for males with an RR of 4.19 (95% CI: 1.81, 9.69) for the IQR difference of 551 h/yr when O3 exceeded 100 parts per billion. Sulfur dioxide showed strong associations with lung cancer mortality for both sexes. Other pollutants showed weak or no association with mortality.

The purpose of this study was to evaluate the relationship of long-term concentrations of ambient air pollutants and risk of incident lung cancer in nonsmoking California adults. A cohort study of 6,338 nonsmoking, non-Hispanic, white Californian adults, ages 27-95, was followed from 1977 to 1992 for newly diagnosed cancers. Monthly ambient air pollution data were interpolated to zip code centroids according to home and work location histories, cumulated, and then averaged over time. The increased relative risk (RR) of incident lung cancer in males associated with an interquartile range (IQR) increase in 100 ppb ozone (O3) was 3.56 [95% confidence interval (CI), 1.35-9.42]. Incident lung cancer in males was also positively associated with IQR increases for mean concentrations of particulate matter <10 microm (PM10; RR = 5.21; CI, 1.94-13.99) and SO2 (RR = 2.66; CI, 1.62-4.39). For females, incident lung cancer was positively associated with IQR increases for SO2 (RR = 2.14; CI, 1.36-3.37) and IQR increases for PM10 exceedance frequencies of 50 microg/m3 (RR = 1.21; CI, 0.55-2.66) and 60 microg/m3 (RR = 1.25; CI, 0.57-2.71). Increased risks of incident lung cancer were associated with elevated long-term ambient concentrations of PM10 and SO2 in both genders and with O3 in males. The gender differences for the O3 and PM10 results appeared to be partially due to gender differences in exposure.

The associations between lung function measures (spirometry and peak expiratory flow lability) and estimated 20-yr ambient concentrations of respirable particles, suspended sulfates, sulfur dioxide, ozone, and indoor particles were studied in a sample of 1,391 nonsmokers followed since 1977. Differences in air pollutants across the population were associated with decrements of lung function. An increase of 54 d/yr when particles < 10 micro(m) in diameter (PM10) exceeded 100 microg/m3 was associated with a 7.2% decrement in FEV1, as percent of predicted, in males whose parents had asthma, bronchitis, emphysema, or hay fever and with increased peak expiratory flow lability of 0.8% for all females and 0.6% for all males. An increase in mean SO4 concentration of 1.6 microg/m3 was associated with a 1.5% decrement in FEV1, as percent of predicted, in all males. An increase of 23 ppb of ozone as an 8-h average was associated with a 6.3% decrement in FEV1, as percent of predicted, in males whose parents had asthma, bronchitis, emphysema, or hay fever.

Methods were developed for estimating fine particulates less than 2.5 microns in aerodynamic diameter (PM2.5) from airport visibility data which detected seasonality and allowed for possible site- and season-specific regressions of PM2.5 on visibility. The methods were applied to nine airports in California in order to produce estimates of PM2.5 for the years 1966-1986 based on 1,767 paired PM2.5/visibility data points where PM2.5 had been measured at a monitoring station near the airport. General F-tests indicated that site- and season-specific regression equations resulted in a statistically significant reduction in residual error. The split halves correlation for estimating PM2.5 from visibility over all areas was 0.82. The methods were used to estimate long-term concentrations of ambient PM2.5 for an epidemiological cohort of 1,868 individuals.

Seventh-Day Adventists (SDAs), nonsmokers who had resided since 1966 in the vicinity of nine airports throughout California (n = 1,868), completed a standardized respiratory symptoms questionnaire in 1977 and again in 1987. For each participant, cumulative ambient concentrations of fine particulates less than 2.5 microns (microns) in aerodynamic diameter (PM2.5) were estimated from airport visibility data. Long-term ambient concentrations of estimated PM2.5 in excess of 20 micrograms per cubic meter (micrograms/m3) were found to be associated with development of definite symptoms of chronic bronchitis between 1977 and 1987. Estimated mean concentrations of PM2.5 were associated with increasing severity of respiratory symptoms related to general airway obstructive disease, chronic bronchitis, and asthma. It was felt that the observed relationships, with the exception of the relationship between increasing severity of chronic bronchitis symptoms and PM2.5, could be due to surrogate relationships with other ambient pollutants.

Site- and season-specific regressions of particulates less than 10 mu in diameter (PM10) on total suspended particulates (TSPs) were formed throughout California during years when both were monitored. The regressions were then applied to monitored TSPs for the years 1973 to 1987, and indirect estimates of PM10 were formed. These estimates of PM10 were validated by interpolating them to other monitoring stations. The split-halves correlation between the estimated and monitored mean concentrations, obtained when both were first cumulated for a 2-y period, was .86. Indirect estimates of PM10 at monitoring stations were interpolated, by month, to zip code centroids of home and work location and were cumulated for a cohort of 3,914 California Seventh-day Adventist (SDA) nonsmokers. Multivariate analyses, adjusted for several covariates, showed statistically significant (p < .05), but small, positive associations between PM10 and development of (a) definite symptoms of overall airway obstructive disease, (b) chronic productive cough, and (c) increased severity of airway obstructive disease and asthma. The relative risk (RR) associated with 1,000 h/y (42 d) exposure to concentrations of PM10 that exceeded 100 micrograms/m3 for development of airway obstructive disease was 1.17 (95% confidence interval [CI]: 1.02, 1.33); for development of productive cough, the RR was 1.21 (CI 1.02, 1.44); and for development of asthma, the RR was 1.30 (CI, 0.97, 1.73). Stronger associations were observed for those who were exposed occupationally to dusts and fumes. The RR of developing airway obstructive disease as an adult for those who had airway obstructive disease as a child was 1.66 (CI 1.15, 2.33).

We attempted to determine the association between occupational and air pollutant exposure with the development of adult asthma through the analysis of a standardized respiratory questionnaire administered to a cohort of 3914 nonsmoking adults in 1977 and again in 1987. Ambient air pollution concentrations were estimated over a 20-year period using monthly interpolations from fixed-site monitoring stations applied to zip code locations by month of residence and work site. Second-hand smoke exposure was significantly associated with the development of asthma (related risk [RR] = 1.45, confidence interval [CI] = 1.21 to 1.75). Airways obstructive disease before age 16 was related to a marked increased risk (RR = 4.24, CI = 4.03 to 4.45). An increased risk of asthma was significantly associated with increased ambient concentrations of ozone exposure in men (RR = 3.12, CI = 1.61 to 5.85).

Seventh-day Adventist nonsmokers, who, subsequent to 1966, had resided within 8 km (5 miles) of their 1977 residence (N = 3,914), completed the National Heart and Lung Institute (NHLI) respiratory symptoms questionnaire in 1977 and again in 1987. For each participant, cumulative ambient concentrations of total suspended particulates (TSP), ozone, and sulfur dioxide (SO2) in excess of several cutoff levels were estimated by month and by interpolating ambient concentrations from state air-monitoring stations to their residential and workplace zip codes for the month. Statistically significant relationships between ambient concentrations of TSP and ozone, but not SO2, were found with several respiratory disease outcomes. Multivariate analyses adjusted for past and passive smoking and occupational exposures. Results are discussed within the context of standards setting for TSP and ozone.

Seventh-day Adventist (SDA) non-smokers who had resided since 1966 within five miles of their 1977 residence (n = 3914) completed a standardized respiratory symptoms questionnaire in 1977 and again in 1987. For each participant, cumulative ambient concentrations from 1977 to 1987 of suspended sulfates (SO4) in excess of several cutoffs as well as mean concentrations were estimated by interpolating monthly ambient concentration statistics from state air monitoring stations to the individual's residential and workplace zip codes. There were significant associations between ambient concentrations of suspended sulfates and development of new cases of asthma, but not new cases of overall airway obstructive disease (AOD) or chronic bronchitis. Comparison of previous analyses, in this population, of respiratory disease symptoms and total suspended particulates (TSP), ozone, and sulfur dioxide (SO2), and multipollutant analyses of these pollutants with SO4, indicated these results were not due to a surrogate relationship with other air pollutants. Development of definite symptoms of AOD and chronic bronchitis was most strongly related to TSP.

Methods for estimating cumulative ambient air pollution concentrations for individuals enrolled in an epidemiological cohort study are described and studied. Monthly interpolations from fixed-site monitoring stations in California to zip code centroids were used. The precision of the interpolation methods for total suspended particulates and ozone was assessed, and fixed-site monitoring stations were used in turn as receptor sites. Actual versus interpolated 2-y mean concentrations did not differ significantly and were correlated with a Pearson correlation coefficient of .78 for total suspended particulates and .87 for ozone. The impact of the change from monitoring total oxidants to ozone on oxidant/ozone cumulations was evaluated, and monthly mean concentrations for total oxidants were compared with ozone for 435 station months during which both pollutants were measured simultaneously. Average concentrations did not differ significantly and were highly correlated (r = 0.94). Exceedance frequency statistics, which averaged slightly higher for ozone than for total oxidants, were also highly correlated.

Cancer incidence and mortality in a cohort of 6000 nonsmoking California Seventh-Day Adventists were monitored for a 6-year period, and relationships with long-term cumulative ambient air pollution were observed. Total suspended particulates (TSP) and ozone were measured in terms of numbers of hours in excess of several threshold levels corresponding to national standards as well as mean concentration. For all malignant neoplasms among females, risk increased with increasing exceedance frequencies of all thresholds of TSP except the lowest one, and those increased risks were highly statistically significant. For respiratory cancers, increased risk was associated with only one threshold of ozone, and this result was of borderline significance. Respiratory disease symptoms were assessed in 1977 and again in 1987 using the National Heart, Lung and Blood Institute respiratory symptoms questionnaire on a subcohort of 3914 individuals. Multivariate analyses which adjusted for past and passive smoking and occupational exposures indicated statistically significantly (p less than 0.05) elevated relative risks ranging up to 1.7 for incidence of asthma, definite symptoms of airway obstructive disease, and chronic bronchitis with TSP in excess of all thresholds except the lowest one but not for any thresholds of ozone. A trend association (p = 0.056) was noted between the threshold of 10 pphm ozone and incidence of asthma. These results are presented within the context of standards setting for these constituents of air pollution.

Risk of chronic obstructive pulmonary disease symptoms due to long-term exposure to ambient levels of total suspended particulates (TSP) and sulfur dioxide (SO2) symptoms was ascertained using the National Heart, Lung, and Blood Institute (NHLBI) respiratory symptoms questionnaire on 7,445 Seventh-Day Adventists. They were non-smokers, at least 25 yr of age, and had lived 11 yr or more in areas ranging from high to low photochemical air pollution in California. Participant cumulative exposures to each pollutant in excess of four thresholds were estimated using monthly residence zip code histories and interpolated dosages from state air monitoring stations. These pollutant thresholds were entered individually and in combination in multiple logistic regression analyses with eight covariables including passive smoking. Statistically significant associations with chronic symptoms were seen for: SO2 exposure above 4 pphm (104 mcg/m3), (p = .03), relative risk 1.18 for 500 hr/yr of exposure; and for total suspended particulates (TSP) above 200 mcg/m3, (p less than .00001), relative risk of 1.22 for 750 hr/yr.

To assess the risk of chronic obstructive pulmonary disease symptoms due to long-term exposure to ambient levels of total oxidants and nitrogen dioxide (NO2), symptoms were ascertained using the National Heart, Lung, and Blood Institute (NHLBI) respiratory symptoms questionnaire. A total of 7,445 Seventh-day Adventist (SDA) nonsmokers who were 25 yr of age or older and had resided at least 11 yr in areas of California with high to low photochemical air pollution were included in this study. Cumulative exposures to each pollutant in excess of four thresholds were estimated for each participant, using zip codes for months of residence and interpolated dosages from state air-monitoring stations. Multiple logistic regression analyses were conducted individually and together for pollutants and included eight covariables, including passive smoking. A statistically significant association with chronic symptoms was seen for total oxidants above 10 pphm (196 mcg/m3) (p less than .004, relative risk of 1.20 for 750 hr/yr). Chronic respiratory disease symptoms were not associated with relatively low NO2 exposure levels in this population. When these pollutant exposures were studied with exposures to total suspended particulates (TSP) and sulfur dioxide (SO2), only TSP exposure above 200 mcg/m3 showed statistical significance (p less than .01). Exposure to TSP is either more strongly associated with symptoms of chronic obstructive pulmonary disease than the other measured exposures or is the best single surrogate representing the mix of pollutants present.

The prevalence of respiratory symptoms, as ascertained by questionnaire, was evaluated in 6,666 nonsmokers who had lived for at least 11 years in either a high photochemical pollution area (4,379 individuals) or a low photochemical pollution area (2,287 individuals). Of these, 5,178 had never smoked, and none was currently smoking. The risk estimate for "definite" COPD, as defined in this study, was 15 percent higher in the high pollution area (p = 0.03), after adjusting for sex, age, race, education, occupational exposure, and past smoking history. Past smokers had a risk estimate 22 percent higher than never smokers (p = 0.01). Multivariate analysis showed a significant effect of air pollution on the prevalence of "definite" COPD which univariate analysis failed to demonstrate.