Do shale oil and gas production activities impact ambient air quality? A comprehensive study of 12 years of chemical concentrations and well production data from the Barnett Shale region of Texas.

Starting around 2008, there was rapid expansion of oil and natural gas (ONG) production into more heavily populated areas within the Dallas-Fort Worth metroplex in the Barnett Shale region of Texas. This colocation raised concerns regarding the effect of ONG activities on chemical levels in the air. In the current study, we examined the potential impacts of ONG activity on the types and concentrations of chemicals in ambient air in the Barnett Shale. Volatile organic compound (VOC) concentrations from 6-12 years (2008-2019) of hourly ambient air monitoring data from 15 monitors (4 monitors had ≥ 10 years of data) were compared to several metrics of ONG activity (number of active wells, natural gas production, condensate production) within a 2-mile radius of each monitor. Monitoring sites were also classified into urban, suburban, and rural areas as a surrogate for nearby vehicular emission sources. Analyses of this huge dataset showed that both peak and mean chemical concentrations of lighter alkane hydrocarbons (e.g., ethane) were most impacted by the number of gas wells. Levels of heavier alkanes (e.g., pentane) were increased by condensate production and at monitors located in areas with greater urbanicity, and therefore higher vehicular emissions. The levels of unsaturated alkynes (e.g., ethylene) were entirely driven by urbanicity and were unaffected by nearby ONG activity. The same pattern was seen with the ratio of iso:n-pentane, which is contrary to the findings of others and suggests an area for future research. Aromatic hydrocarbons were impacted by multiple emissions sources and did not show the same patterns as non-aromatic VOCs. No VOC concentrations were at levels of concern for human health or odor based on comparison to Texas air monitoring comparison values. Overall, ONG activities impact air quality, but this must be evaluated in the context of other emission sources such as automobiles.

Development of an inhalation reference concentration for diethanolamine.

An inhalation reference concentration (RfC) was developed for diethanolamine (DEA), based principally on evaluation of three animal studies (Gamer et al., 1993, 1996, 2008). The RfC (25 µg/m3) was based on statistically significantly increased relative liver weight in female rats in Gamer et al. (2008) as the critical effect. The lower confidence limit on the benchmark dose (BMDL10 of 5.5 mg/m3) was adjusted to a human equivalent concentration and to continuous exposure before dividing the final point of departure (2.3 mg/m3) by a total factor of 90 that considered standard key areas of uncertainty (intrahuman variability, potential interspecies toxicodynamic differences, database limitations). While laryngeal effects observed in Gamer et al. (2008) were also considered as candidate critical effects, evaluation of the adversity and human relevance of rat laryngeal squamous metaplasia and concomitant effects at the various exposure levels resulted in identifying a LOAEL for laryngeal squamous hyperplasia and chronic inflammation that was much higher than the liver weight LOAEL identified. The RfC of 25 µg/m3 is considered health protective for the general population and can be used to evaluate the potential health effects of long-term environmental exposure of the general public (i.e., long-term, ambient air dispersion modelling or monitoring data).

The perpetuation of the misconception that rats receive a 3-5 times lower lung tissue dose than humans at the same ozone concentration.

This paper highlights the pervasive misconception concerning 1994 findings from Hatch et al. about ozone (O3) tissue dose in humans versus rats. That study exposed humans to 0.4 ppm and rats to 2 ppm 18O-labeled O3 and found comparable incorporation of 18O into bronchoalveolar lavage constituents. However, during O3 exposure humans were exercising, which increased their ventilation rate five-fold, while rats were at rest. This resulted in similar O3 tissue doses between the two species, and predominantly explained the comparable 18O incorporation at five-fold different concentrations. The five-times higher exercising human inhalation rate offset the five-times lower concentration, producing the same human dose expected at rest at 2 ppm (i.e. 0.4 ppm × 4686 L/2 hour ≈ 2 ppm × 998 L/2 hour). In 2013, Hatch et al. showed that resting humans and resting rats experienced fairly comparable 18O incorporation at the same O3 exposure concentration and activity state into BALF cells. Despite these findings, we show here that in the peer-reviewed literature a substantial proportion of researchers continue to perpetuate the misunderstanding that human lung tissue doses of O3 are simply 3-5 times greater than rat doses at the same O3 concentration, due to interspecies differences, and not considering activity state. It is important to correct this misconception to ensure an appropriate understanding of the implications of O3 studies by the scientific community and policy experts making regulatory decisions (e.g. the US Environmental Protection Agency's National Ambient Air Quality Standards for O3).

Assessment of chronic inhalation non-cancer toxicity for diethylamine.

A non-cancer inhalation chronic toxicity assessment for diethylamine (DEA, CAS number 109-89-7) was conducted by the Texas Commission on Environmental Quality. A chronic Reference Value (ReV) was determined based on a high-quality study conducted in mice and rats by the National Toxicology Program. Chronic inhalation ReVs are health-based exposure concentrations used in assessing health risks of long-term (i.e. lifetime) chemical exposure. DEA is used industrially as an organic intermediate to produce corrosion inhibitors, and is widely used in rubber, pharmaceuticals, resins, pesticides, insect repellants, dye processing and as a polymerization inhibitor. Although systemic effects have been noted at higher concentrations, DEA acts primarily as a respiratory irritant with effects occurring in the upper respiratory tract. Rats were exposed to 0, 31, 62.5 and 125 ppm DEA and mice to 0, 16, 31 and 62.5 ppm DEA for 6 h/day, 5 days/week for 105 weeks. Mice were slightly more sensitive than rats. The critical effect identified in mice was hyperostosis in the turbinates although DEA caused a number of other non-neoplatic lesions. Dose-response data were suitable to benchmark concentration (BMC) modeling. The human equivalent point of departure (PODHEC) was calculated from the 95% lower limit of the BMC(10) using default duration and animal-to-human dosimetric adjustments. Total uncertainty factors of 90 were applied to the PODHEC to account for variation in sensitivity within the human population, toxicodynamic differences between mice and humans, and database uncertainty. The chronic ReV for DEA is 11 ppb (33 µg/m(3)).

Impact of three interactive Texas state regulatory programs to decrease ambient air toxic levels.

UNLABELLED: The Federal Clean Air Act (FCAA) framework envisions a federal-state partnership whereby the development of regulations may be at the federal level or state level with federal oversight. The US. Environmental Protection Agency (EPA) establishes National Ambient Air Quality Standards to describe "safe" ambient levels of criteria pollutants. For air toxics, the EPA establishes control technology standards for the 187 listed hazardous air pollutants (HAPs) but does not establish ambient standards for HAPs or other air toxics. Thus, states must ensure that ambient concentrations are not at harmful levels. The Texas Clean Air Act authorizes the Texas Commission on Environmental Quality (TCEQ), the Texas state environmental agency, to control air pollution and protect public health and welfare. The TCEQ employs three interactive programs to ensure that concentrations of air toxics do not exceed levels of potential health concern (LOCs): air permitting, ambient air monitoring, and the Air Pollutant Watch List (APWL). Comprehensive air permit reviews involve the application of best available control technology for new and modified equipment and ensure that permits protect public health and welfare. Protectiveness may be demonstrated by a number of means, including a demonstration that the predicted ground-level concentrations for the permitted emissions, evaluated on a case-by-case and chemical-by-chemical basis, do not cause or contribute to a LOC. The TCEQ's ambient air monitoring program is extensive and provides data to help assess the potential for adverse effects from all operational equipment in an area. If air toxics are persistently monitored at a LOC, an APWL area is established. The purpose of the APWL is to reduce ambient air toxic concentrations below LOCs by focusing TCEQ resources and heightening awareness. This paper will discuss examples of decreases in air toxic levels in Houston and Corpus Christi, Texas, resulting from the interactive nature of these programs. IMPLICATIONS: Texas recognized through the collection of ambient monitoring data that additional measures beyond federal regulations must be taken to ensure that public health is protected. Texas integrates comprehensive air permitting, extensive ambient air monitoring, and the Air Pollutant Watch List (APWL) to protect the public from hazardous air toxics. Texas issues air permits that are protective of public health and also assesses ambient air to verify that concentrations remain below levels of concern in heavily industrialized areas. Texas developed the APWL to improve air quality in those areas where monitoring indicates a potential concern. This paper illustrates how Texas engaged its three interactive programs to successfully address elevated air toxic levels in Houston and Corpus Christi.

Development of a unit risk factor for nickel and inorganic nickel compounds based on an updated carcinogenic toxicity assessment.

The TCEQ has developed a URF for nickel based on excess lung cancer in two epidemiological studies of nickel refinery workers with nickel species exposure profiles most similar to emissions expected in Texas (i.e., low in sulfidic nickel). One of the studies (Enterline and Marsh, 1982) was used in the 1986 USEPA assessment, while the other (Grimsrud et al., 2003) is an update to an earlier study (Magnus et al., 1982) used by USEPA. The linear multiplicative relative risk model with Poisson regression modeling was used to obtain maximum likelihood estimates and asymptotic variances for cancer potency factors (ß) using cumulative nickel exposure levels versus observed and expected lung cancer mortality (Enterline and Marsh, 1982) or lung cancer incidence cases (Grimsrud et al., 2003). Life-table analyses were then used to develop URFs from these two studies, which were combined using weighting factors relevant to confidence to derive the final URF for nickel of 1.7E-04 per µg/m³. The de minimis air concentration corresponding to a 1 in 100,000 extra lung cancer risk level is 0.059 µg/m³. The TCEQ will use this conservative value to protect the general public in Texas against the potential carcinogenic effects from chronic exposure to nickel.

Spatial and temporal trend evaluation of ambient concentrations of 1,3-butadiene and chloroprene in Texas.

This paper provides information on 1,3-butadiene (BD) and chloroprene as atmospheric pollutants in Texas and reviews available emission estimates and monitoring data. Ambient BD concentrations in most areas of Texas are predominantly influenced by on-road and off-road vehicular emissions or biomass burning, since BD is a product of combustion. However, large industrial point sources of BD emissions in Texas locally influence ambient concentrations. Total industrial BD emissions to the atmosphere in Texas for 2003 were estimated at 695 tonnes per year (TPY), approximately 70% of the total reported national industrial BD air emissions. Since 1998, there have not been any large industrial sources of chloroprene emissions in Texas, and total industrial chloroprene emissions for 2003 was estimated at only 0.09 TPY. Chloroprene was never detected at air monitoring sites. In 2003, the Texas Commission on Environmental Quality (TCEQ) monitored BD ambient air concentrations at 57 sites, some of which have been operational since 1992. These air monitors provide information on ambient BD concentrations in Texas and allow spatial and temporal trend evaluation. In 2003, annual average concentrations at monitoring sites in Texas ranged from less than the reporting limit of 0.01 to 3.2 parts per billion by volume (ppbv) with an overall average of 0.2 ppbv. This overall average is reduced to 0.1 ppbv if BD data from monitoring sites in Port Neches and Milby Park in Houston, which are located downwind of significant point sources of BD, are excluded. Ambient air monitoring has been conducted in Port Neches and in Milby Park in Houston since 1996 and 1999, respectively. At the Port Neches monitor, trend evaluation indicates that ambient concentrations of BD have declined since 1996 due to cooperative agreements with industries emitting BD. Annual average BD concentrations at the Port Neches monitor decreased from 8.3ppbv in 1996 to 1.3 ppbv in 2003, giving an 8-year average of 3.8 ppbv. Annual average BD concentrations at the Milby Park monitor varied between 2.1 and 4.4 ppbv from 1999 through 2003, giving a 5-year average of 3.1 ppbv. The results of cancer cluster studies based on Cancer Registry 1995-2001 incidence data and 1993-2002 mortality data conducted by the Texas Department of State Health Services for zip codes 77017/77012 (Houston) and 77651 (Port Neches) will be presented.