Environ. Sci. Technol. 2007, 41, 1038-1043
Inhalation Health Risk to Golfers from Turfgrass Pesticides at Three Northeastern U.S. Sites REBECCA R. MURPHY AND DOUGLAS A. HAITH* Biological and Environmental Engineering, Riley-Robb Hall, Cornell University, Ithaca, New York 14853
Chronic health risks from inhalation of vapors from 15 pesticides were estimated for golfers in Boston, MA, Philadelphia, PA, and Rochester, NY. Two previously tested fate and transport models were used to determine exposures from pesticide inhalation for an adult golfer, and the exposures were in turn used to evaluate health risks from chronic non-carcinogenic effects through calculation of hazard quotients. Hazard quotients for all 15 chemicals were found to be much less one, indicating little risk of noncarcinogenic effects. Carcinogenic health risks for the five pesticides considered to be likely or possible carcinogens were determined to be much less than 10-6. Based on these results, long-term health risks to golfers from inhalation of these 15 pesticides appear to be minimal in the Northeastern U.S. Estimated hazard quotients were found to be similar to those calculated from field measurements.
Introduction Pesticides applied to golf courses may impact both the environment and human health. Cohen et al. (1) reviewed monitoring studies of water quality near golf courses, and found that 31 pesticides have been detected in surface waters on or near golf courses. Haith and Rossi (2) determined that concentrations of several turf pesticides in runoff from golf greens and fairways often exceeded concentrations associated with 50% mortality of rainbow trout and Daphnia magna. Murphy et al. (3, 4) and Clark et al. (5) found that ethoprop, diazinon, and isazofos were potentially hazardous to golfers based on inhalation doses calculated from measured pesticide residues in the air. These same three pesticides plus a fourth, isofenphos, were found to pose health risks from the dermal exposure route. Cohen et al. (6) sampled groundwater at four golf courses on Cape Cod, MA. Seven pesticides were detected in the samples, and calculated exposures were found to exceed guidance levels for one of the pesticides. Pesticide applications to golf courses may produce human health risks from inhalation, ingestion, and dermal contact. Because of their proximity to the chemicals, golfers are especially susceptible to inhalation exposure. Pesticides are routinely applied to maintain the quality of playing surfaces, and it is impractical to keep golfers from the affected areas long enough for complete dissipation of the vapors. Some protection is provided by reentry intervals, but these time periods are of necessity short for golf course pesticides. Although the three pesticides which were found to have inhalation health hazards in the Murphy et al. and Clark et * Corresponding author phone: 607-255-2802; fax: 607-255-4080; e-mail:
[email protected]. 1038
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al. studies have been cancelled or withdrawn from use on golf courses, there have been no systematic studies of the inhalation hazards associated with the large number of other pesticides applied to golf courses. In this paper, we describe the results of an assessment of inhalation health risk for 15 pesticides typically applied to golf courses in the northeastern U.S. Three locations were considered, Boston, Philadelphia, and Rochester. Fate and transport models were used to determine exposures from pesticide inhalation for an adult golfer, and the exposures were in turn used to evaluate health risks from chronic noncarcinogenic effects through calculation of hazard quotients. Carcinogenic health effects were determined by estimating a golfer’s incremental cancer risk.
Materials and Methods Measures of Risk and Exposure. Assessment of the health risk of a chemical requires comparison of an exposure, or intake dose for a targeted person with an appropriate health criterion. The lifetime average daily dose (LADD, mg kg-1 d-1) is generally the exposure measure for both carcinogenic and chronic non-carcinogenic hazard. A chronic noncarcinogenic effect is captured by a reference dose (RfD, mg kg-1 d-1), which is considered the daily exposure over a 70year life span which produces no harmful effects. Following Murphy et al. (3, 4), we can use a hazard quotient,
HQ ) LADD/RfD
(1)
to describe the extent of chronic risk. Chemicals with HQ < 1 would be considered relatively safe, at least with regard to non-cancerous health effects. For carcinogens, a linear dose response, described by cancer slope or potency factor, Q* (kg d mg-1), is multiplied by LADD to estimate an individual’s incremental probability of contracting cancer. Incremental lifetime cancer risk is thus
ICR ) LADD Q*
(2)
An ICR value greater than 1.0 10-6 (one in a million) is generally unacceptable (7). Chronic RfD or comparable ADI (allowable daily intake) and Q* values for most pesticides are available from National Pesticide Information Center (8). The lifetime average daily dose for a 70-kg golfer playing a daily round is
LADD ) (0.001 b d/70) Cav
(3)
where Cav is the average daily ambient concentration of the chemical in air (µg m-3), b ) breathing rate (m3 h-1), and d ) duration of exposure (h). Equation 3 assumes complete absorption of the pollutant. The factor “0.001” converts the µg units of Cav to mg. Exposures are sometimes estimated as a lifetime maximum daily dose, as in Murphy et al. (3, 4) and Clark et al. (5):
LMDD ) (0.001 b d/70) Cmax
(4)
with Cmax equal to the maximum measured daily concentration. Although this would appear to produce a very unlikely (and extremely conservative) dose, it provides a convenient upper-bound on lifetime exposure. Fate and Transport Models. Fate and transport models can simulate a range of conditions, corresponding to different weather and sites. They are often run with long-term average weather data, thus providing concentrations suitable for 10.1021/es060964b CCC: $37.00
2007 American Chemical Society Published on Web 12/14/2006
determining average exposure doses. Yates (9) combined a soil root zone solute model with a trajectory simulation atmospheric transport model (10) to estimate off-site concentrations of an agricultural pesticide. A comparable approach can be taken with turf pesticides. The turf pesticide volatilization model developed by Haith et al. (11) and modified by Walden and Haith (12) provides estimates of volatilization mass flux from a turf surface, and concentrations can be determined from solutions to the trajectory simulation model. Volatilization Flux. The first step in determining pesticide vapor concentrations is estimation of volatilization mass flux, using the daily evapotranspiration (ET) based model proposed and tested by Walden and Haith (12):
Vt ) kETt (psct/pswt) (λwt/λct) (Pt + ∆Pt)
(5)
where Vt ) volatilized pesticide during day t (g ha-1 d-1), ETt ) ET during day t (mm d-1), Pt ) pesticide on the turf at the beginning of day t (g ha-1), ∆Pt ) pesticide application on day t (g ha- 1), k ) volatilization coefficient (mm-1), psct ) chemical saturated vapor pressure on day t (kPa), pswt ) water saturated vapor pressure on day t (kPa), λct ) latent heat of vaporization of the chemical during day t (J g-1), and λwt ) latent heat of vaporization of water on day t (J g-1). Equations for determining psct, pswt, λwt, and λct as functions of air temperature are given in Walden and Haith (12). Values of the volatilization coefficient k were determined by Haith et al. (11) through a calibration process using measured volatilization fluxes. Model performance differed markedly depending on vapor pressure, and values of the coefficient were determined for two different groups of pesticides: k ) 405 mm-1 for vapor pressures
