Fine Particulate Matter and Lung Function among Burning-Exposed Deepwater Horizon Oil Spill Workers

BACKGROUND: During the 2010 Deepwater Horizon (DWH) disaster, controlled burning was conducted to remove oil from the water. Workers near combustion sites were potentially exposed to increased fine particulate matter [with aerodynamic diameter ≤2:5 lm (PM2:5 )] levels. Exposure to PM2:5 has been linked to decreased lung function, but to our knowledge, no study has examined exposure encountered in an oil spill cleanup. OBJECTIVE: We investigated the association between estimated PM2:5 only from burning/flaring of oil/gas and lung function measured 1–3 y after the DWH disaster. METHODS: We included workers who participated in response and cleanup activities on the water during the DWH disaster and had lung function measured at a subsequent home visit (n = 2,316). PM2:5 concentrations were estimated using a Gaussian plume dispersion model and linked to work histories via a job-exposure matrix. We evaluated forced expiratory volume in 1 s (FEV1; milliliters), forced vital capacity (FVC; milliliters), and their ratio (FEV1/FVC; %) in relation to average and cumulative daily maximum exposures using multivariable linear regressions. RESULTS: We observed significant exposure–response trends associating higher cumulative daily maximum PM2:5 exposure with lower FEV1 (p-trend = 0:04) and FEV1/FVC (p-trend = 0:01). In comparison with the referent group (workers not involved in or near the burning), those with higher cumulative exposures had lower FEV1 [−166:8 mL, 95% confidence interval (CI): −337:3, 3.7] and FEV1/FVC (−1:7, 95% CI: −3:6, 0.2). We also saw nonsignificant reductions in FVC (high vs. referent: −120:9, 95% CI: −319:4, 77.6; p-trend = 0:36). Similar associations were seen for average daily maximum PM2:5 exposure. Inverse associations were also observed in analyses stratified by smoking and time from exposure to spirom-etry and when we restricted to workers without prespill lung disease. CONCLUSIONS: Among oil spill workers, exposure to PM2:5 specifically from controlled burning of oil/gas was associated with significantly lower FEV1 and FEV1/FVC when compared with workers not involved in burning. https://doi.org/10.1289/EHP8930

Associations between airborne crude oil chemicals and symptom-based asthma

Rationale: The 2010 Deepwater Horizon (DWH) oil spill response and cleanup (OSRC) workers were exposed to airborne total hydrocarbons (THC), benzene, toluene, ethylbenzene, o-, m-, and p-xylenes and n-hexane (BTEX-H) from crude oil and PM2.5 from burning/flaring oil and natural gas. Little is known about asthma risk among oil spill cleanup workers. Objectives: We assessed the relationship between asthma and several oil spill-related exposures including job classes, THC, individual BTEX-H chemicals, the BTEX-H mixture, and PM2.5 using data from the Gulf Long-Term Follow-up (GuLF) Study, a prospective cohort of 24,937 cleanup workers and 7,671 nonworkers following the DWH disaster. Methods: Our analysis largely focused on the 19,018 workers without asthma before the spill who had complete exposure, outcome, and covariate information. We defined incident asthma 1–3 years following exposure using both self-reported wheeze and self-reported physician diagnosis of asthma. THC and BTEX-H were assigned to participants based on measurement data and work histories, while PM2.5 used modeled estimates. We used modified Poisson regression to estimate risk ratios (RR) and 95% confidence intervals (CIs) for associations between spill-related exposures and asthma and a quantile-based g-computation approach to explore the joint effect of the BTEX-H mixture on asthma risk. Results: OSRC workers had greater asthma risk than nonworkers (RR: 1.60, 95% CI: 1.38, 1.85). Higher estimated THC exposure levels were associated with increased risk in an exposure-dependent manner (linear trend test p < 0.0001). Asthma risk also increased with increasing exposure to individual BTEX-H chemicals and the chemical mixture: A simultaneous quartile increase in the BTEX-H mixture was associated with an increased asthma risk of 1.45 (95% CI: 1.35,1.55). With fewer cases, associations were less apparent for physician-diagnosed asthma alone. Conclusions: THC and BTEX-H were associated with increased asthma risk defined using wheeze symptoms as well as a physician diagnosis

Association of Deepwater Horizon Oil Spill Response and Cleanup Work With Risk of Developing Hypertension

Importance: Exposure to hydrocarbons, fine particulate matter (PM2.5), and other chemicals from the April 20, 2010, Deepwater Horizon disaster may be associated with increased blood pressure and newly detected hypertension among oil spill response and cleanup workers. Objective: To determine whether participation in cleanup activities following the disaster was associated with increased risk of developing hypertension. Design, Setting, and Participants: This cohort study was conducted via telephone interviews and in-person home exams. Participants were 6846 adults who had worked on the oil spill cleanup (workers) and 1505 others who had completed required safety training but did not do cleanup work (nonworkers). Eligible participants did not have diagnosed hypertension at the time of the oil spill. Statistical analyses were performed from June 2018 to December 2021. Exposures: Engagement in cleanup activities following the Deepwater Horizon oil spill disaster, job classes, quintiles of cumulative total hydrocarbons exposure level, potential exposure to burning or flaring oil, and estimated PM2.5were examined. Main Outcomes and Measures: Systolic and diastolic blood pressure measurements were collected during home exams from 2011 to 2013 using automated oscillometric monitors. Newly detected hypertension was defined as antihypertensive medication use or elevated blood pressure since the spill. Log binomial regression was used to calculate prevalence ratios (PR) and 95% CIs for associations between cleanup exposures and hypertension. Multivariable linear regression was used to estimate exposure effects on continuous blood pressure levels. Results: Of 8351 participants included in this study, 6484 (77.6%) were male, 517 (6.2%) were Hispanic, 2859 (34.2%) were non-Hispanic Black, and 4418 (52.9%) were non-Hispanic White; the mean (SD) age was 41.9 (12.5) years at enrollment. Among workers, the prevalence of newly detected hypertension was elevated in all quintiles (Q) of cumulative total hydrocarbons above the first quintile (PR for Q3, 1.29 [95% CI, 1.13-1.46], PR for Q4, 1.25 [95% CI, 1.10-1.43], and PR for Q5, 1.31 [95% CI, 1.15-1.50]). Both exposure to burning and/or flaring oil and gas (PR, 1.16 [95% CI, 1.02-1.33]) and PM2.5from burning (PR, 1.26 [95% CI, 0.89-1.71]) for the highest exposure category were associated with increased risk of newly detected hypertension, as were several types of oil spill work including cleanup on water (PR, 1.34 [95% CI, 1.08-1.66]) and response work (PR, 1.51 [95% CI, 1.20-1.90]). Conclusions and Relevance: Oil spill exposures were associated with newly detected hypertension after the Deepwater Horizon disaster. These findings suggest that blood pressure screening should be considered for workers with occupational hydrocarbon exposure

Fine particulate matter and incident coronary heart disease events up to 10 years of follow-up among Deepwater Horizon oil spill workers

Background: During the 2010 Deepwater Horizon (DWH) disaster, in-situ burning and flaring were conducted to remove oil from the water. Workers near combustion sites were potentially exposed to burning-related fine particulate matter (PM2.5). Exposure to PM2.5 has been linked to increased risk of coronary heart disease (CHD), but no study has examined the relationship among oil spill workers. Objectives: To investigate the association between estimated PM2.5 from burning/flaring of oil/gas and CHD risk among the DWH oil spill workers. Methods: We included workers who participated in response and cleanup activities on the water during the DWH disaster (N = 9091). PM2.5 exposures were estimated using a job-exposure matrix that linked modelled PM2.5 concentrations to detailed DWH spill work histories provided by participants. We ascertained CHD events as the first self-reported physician-diagnosed CHD or a fatal CHD event that occurred after each worker's last day of burning exposure. We estimated hazard ratios (HR) and 95% confidence intervals (95%CI) for the associations between categories of average or cumulative daily maximum PM2.5 exposure (versus a referent category of water workers not near controlled burning) and subsequent CHD. We assessed exposure-response trends by examining continuous exposure parameters in models. Results: We observed increased CHD hazard among workers with higher levels of average daily maximum exposure (low vs. referent: HR = 1.26, 95% CI: 0.93, 1.70; high vs. referent: HR = 2.11, 95% CI: 1.08, 4.12; per 10 μg/m3 increase: HR = 1.10, 95% CI: 1.02, 1.19). We also observed suggestively elevated HRs among workers with higher cumulative daily maximum exposure (low vs. referent: HR = 1.19, 95% CI: 0.68, 2.08; medium vs. referent: HR = 1.38, 95% CI: 0.88, 2.16; high vs. referent: HR = 1.44, 95% CI: 0.96, 2.14; per 100 μg/m3-d increase: HR = 1.03, 95% CI: 1.00, 1.05). Conclusions: Among oil spill workers, exposure to PM2.5 from flaring/burning of oil/gas was associated with increased risk of CHD

Hsp90-binding immunophilins link p53 to dynein during p53 transport to the nucleus

The tumor suppressor protein p53 is known to be transported to the nucleus along microtubular tracks by cytoplasmic dynein. However, the connection between p53 and the dynein motor protein complex has not been established. Here, we show that hsp90·binding immunophilins link p53·hsp90 complexes to dynein and that prevention of that linkage in vivo inhibits the nuclear movement of p53. First, we show that p53·hsp90 heterocomplexes from DLD-1 human colon cancer cells contain an immunophilin (FKBP52, CyP-40, or PP5) as well as dynein. p53·hsp90·immunophilin·dynein complexes can be formed by incubating immunopurified p53 with rabbit reticulocyte lysate, and we show by peptide competition that the immunophilins link via their tetratricopeptide repeat domains to p53-bound hsp90 and by means of their PPIase domains to the dynein complex. The linkage of immunophilins to the dynein motor is indirect by means of the dynamitin component of the dynein-associated dynactin complex, and we show that purified FKBP52 binds directly by means of its PPIase domain to purified dynamitin. By using a temperature-sensitive mutant of p53 where cytoplasmic-nuclear movement occurs by shift to permissive temperature, we show that p53 movement is impeded when p53 binding to hsp90 is inhibited by the hsp90 inhibitor radicicol. Also, nuclear movement of p53 is inhibited when immunophilin binding to dynein is competed for by expression of a PPIase domain fragment in the same manner as when dynein linkage to cargo is dissociated by expression of dynamitin. This is the first demonstration of the linkage between an hsp90-chaperoned transcription factor and the system for its retrograde movement to the nucleus both in vitro and in vivo