As an agricultural country and one of the world’s major food exporters, Thailand relies heavily on the use of pesticides to protect crops and increase yields. During the past decade, the Kingdom of Thailand has experienced an approximate four-fold increase in pesticide use. This increase presents a challenge for the Royal Thai Government in effectively managing and controlling pesticide use based upon the current policies and legal infrastructure. We have reviewed several key components for managing agricultural pesticides in Thailand. One of the main obstacles to effective pesticide regulation in Thailand is the lack of a consolidated, uniform system designed specifically for pesticide management. This deficit has weakened the enforcement of existing regulations, resulting in misuse/overuse of pesticides, and consequently, increased environmental contamination and human exposure. This article provides a systematic review of how agricultural pesticides are regulated in Thailand. In addition, we provide our perspectives on the current state of pesticide management, the potential health effects of widespread, largely uncontrolled use of pesticides on the Thai people and ways to improve pesticide management in Thailand.

Background: Few data exist in Latin America concerning the association between organophosphate (OP) urinary metabolites and the consumption of fruits and vegetables and other exposure risk variables in schoolchildren. Methods: We collected samples of urine from 190 Chilean children aged 6-12. years, fruits and vegetables, water and soil from schools and homes, and sociodemographic data through a questionnaire. We measured urinary dialkylphosphate (DAP) OP metabolites and OP pesticide residues in food consumed by these 190 children during two seasons: December 2010 (summer) and May 2011 (fall). We analyzed the relationship between urinary DAP concentrations and pesticide residues in food, home pesticide use, and residential location. Results: Diethylalkylphosphates (DEAP) and dimethylalkylphosphates (DMAP) were detected in urine in 76% and 27% of the samples, respectively. Factors associated with urinary DEAP included chlorpyrifos in consumed fruits (. p < . 0.0001), urinary creatinine (. p < . 0.0001), rural residence (. p=. 0.02) and age less than 9. years (. p=. 0.004). Factors associated with urinary DMAP included the presence of phosmet residues in fruits (. p < . 0.0001), close proximity to a farm (. p=. 0.002), home fenitrothion use (. p=. 0.009), and season (. p < . 0.0001). Conclusions: Urinary DAP levels in Chilean school children were high compared to previously reported studies. The presence of chlorpyrifos and phosmet residues in fruits was the major factor predicting urinary DAP metabolite concentrations in children.

Since urinary insecticide metabolites are commonly used as biomarkers of exposure, it is important that we quantify whether insecticides degrade in food and beverages in order to better perform risk assessment. This study was designed to quantify degradation of organophosphorus and pyrethroid insecticides in beverages. Purified water, white grape juice, orange juice, and red wine were fortified with 500 ng/mL diazinon malathion, chlorpyrifos, permethrin, cyfluthrin, cypermethrin, and deltamethrin, and aliquots were extracted several times over a 15-day storage period at 2.5 °C. Overall statistically significant loss of at least one insecticide was observed in each matrix, and at least five out of seven insecticides demonstrated a statistically significant loss in all matrices except orange juice. An investigation of an alternative mechanism of insecticide loss-adsorption onto the glass surface of the storage jars-was carried out, which indicated that this mechanism of loss is insignificant. Results of this work suggest that insecticides degrade in these beverages, and this degradation may lead to pre-existing insecticide degradates in the beverages, suggesting that caution should be exercised when using urinary insecticide metabolites to assess exposure and risk.

Background Although the susceptibility of the developing fetus to various chemical exposures is well documented, the role of environmental chemicals in childhood brain cancer etiology is not well understood. Objectives We aimed to evaluate whether mothers of childhood brain cancer cases had greater potential residential exposure to Toxics Release Inventory (TRI) chemicals than control mothers during pregnancy. Methods We included 382 brain cancer cases diagnosed at < 10 years of age from 1993 through 1997 who were identified from four statewide cancer registries. One-to-one matched controls were selected by random-digit dialing. Computer-assisted telephone interviews were conducted. Using residential history of mothers during pregnancy, we measured proximity to TRI facilities and exposure index, including mass and chemicals released. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression to estimate brain cancer risk associated with TRI chemicals. Results Increased risk was observed for mothers living within 1 mi of a TRI facility (OR = 1.66; 95% CI, 1.11–2.48) and living within 1 mi of a facility releasing carcinogens (OR = 1.72; 95% CI, 1.05–2.82) for having children diagnosed with brain cancer before 5 years of age, compared to living > 1 mi from a facility. Taking into account the mass and toxicity of chemical releases, we found a nonsignificant increase in risk (OR = 1.25; 95% CI, 0.67–2.34) comparing those with the lowest versus highest exposure index. Conclusions Risk of childhood brain cancers may be associated with living near a TRI facility; however, this is an exploratory study and further studies are needed.

To address the lack of research on the pulmonary health effects of ozone and fine particulate matter (≤ 2.5 μm in aerodynamic diameter; PM2.5) on individuals who recreate in the Great Smoky Mountains National Park (USA) and to replicate a study performed at Mt. Washington, New Hampshire (USA), we conducted an observational study of adult (18–82 years of age) day hikers of the Charlies Bunion trail during 71 days of fall 2002 and summer 2003. Volunteer hikers performed pre- and posthike pulmonary function tests (spirometry), and we continuously monitored ambient O3, PM2.5, temperature, and relative humidity at the trailhead. Of the 817 hikers who participated, 354 (43%) met inclusion criteria (nonsmokers and no use of bronchodilators within 48 hr) and gave acceptable and reproducible spirometry. For these 354 hikers, we calculated the posthike percentage change in forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), FVC/FEV1, peak expiratory flow, and mean flow rate between 25 and 75% of the FVC and regressed each separately against pollutant (O3 or PM2.5) concentration, adjusting for age, sex, hours hiked, smoking status (former vs. never), history of asthma or wheeze symptoms, hike load, reaching the summit, and mean daily temperature. O3 and PM2.5 concentrations measured during the study were below the current federal standards, and we found no significant associations of acute changes in pulmonary function with either pollutant. These findings are contrasted with those in the Mt. Washington study to examine the hypothesis that pulmonary health effects are associated with exposure to O3 and PM2.5 in healthy adults engaged in moderate exercise.

Organophosphate (OP) pesticides are widely used for crop protection in many countries including Thailand. Aside from causing environmental contamination, they affect human health especially by over-stimulating of the neurotransmission system. OP pesticides, as with other non-persistent pesticides, degrade quickly in the environment as well as are metabolized quite rapidly in humans. Assessing human exposures to these compounds requires analytical methods that are sensitive, robust, and most importantly, suitable for specific laboratory settings. The aim of this study was to develop and validate an analytical method for measuring 11 OP pesticide residues in human plasma and breast milk. Analytes in both plasma and breast milk samples were extracted with acetone and methylene chloride, cleaned-up using aminopropyl solid phase extraction cartridges, and analyzed by gas chromatography with flame photometric detection. The optimized method exhibited good linearity, with the coefficients of determination of 0.996-0.999 and <7% error about the slope. Extraction recoveries from spiked plasma and breast milk samples at low and medium concentrations (0.8-5.0 and 1.6-10 ng mL-1, respectively) ranged from 59.4% (ethion) to 94.0% (chlorpyrifos). Intra-batch and inter-batch precisions ranged from 2.3-18.9% and 5.8-19.5%, respectively. Method detection limits of plasma and breast milk ranged from 0.18-1.36 and 0.09-2.66 ng mL-1, respectively. We analyzed 63 plasma and 30 breastmilk samples collected from farmworkers in Chiang Mai Province to determine the suitability of this method for occupational exposure assessment. Of the 11 pesticides measured, seven were detected in plasma samples and five were detected in breast milk samples. Mass spectrometry was used to confirm results. Overall, this method is rapid and reliable. It offers the laboratories with limited access to mass spectrometry a capacity to investigate levels OP pesticides in plasma and breastmilk in those occupationally exposed for health risk assessment.

Background: 3-Phenoxybenzoic acid (3PBA), a pyrethroid metabolite, was detected in 75% of urine samples analyzed for pesticides in the U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2002. NHANES also includes 24-hr diet data and information on household pesticide use, activities, occupation, demographics, and other exposure factors. Objectives: The objective of our study was to explore the relative importance of diet versus nondiet predictors in explaining variability in urinary 3PBA. A secondary objective was to explore whether the NHANES data could be used to identify particular foods driving 3PBA levels. Methods: We divided subjects into child (6–10 years of age), teen (11–18 years), and adult (≥ 19 years) age groups and restricted our analyses to subjects in the morning sampling session who fasted for ≥ 8 hr beforehand. Regression modeling consisted of several model-building steps and a final Tobit regression on the left-censored log 3PBA measurements. We also conducted bootstrap analyses to evaluate the stability of the regression parameters. Results: Reported household pesticide use was not significantly associated with urinary 3PBA in any age group. Diet was significant for all three groups, and certain foods appeared to contribute more than others. Among adults, tobacco use was positively associated with 3PBA (p = 0.0326), and positive associations were suggested with the number of cytochrome p450–inhibiting medications taken (p = 0.0652) and minutes spent gardening (p = 0.0613) in the past month. Conclusions: Although exploratory, our findings underline the importance of collecting accurate data on household pesticide use and dietary intake when evaluating pyrethroid exposure–biomarker relationships.

Background: People living or working in eastern Ohio and western West Virginia have been exposed to perfluorooctanoic acid (PFOA) released by DuPont Washington Works facilities. Objectives: Our objective was to estimate historical PFOA exposures and serum concentrations experienced by 45,276 non-occupationally exposed participants in the C8 Health Project who consented to share their residential histories and a 2005-2006 serum PFOA measurement. Methods: We estimated annual PFOA exposure rates for each individual based on predicted calibrated water concentrations and predicted air concentrations using an environmental fate and transport model, individual residential histories, and maps of public water supply networks. We coupled individual exposure estimates with a one-compartment absorption, distribution, metabolism, and excretion (ADME) model to estimate time-dependent serum concentrations. Results: For all participants (n = 45,276), predicted and observed median serum concentrations in 2005-2006 are 14.2 and 24.3 ppb, respectively [Spearman's rank correlation coefficient (r s ) = 0.67]. For participants who provided daily public well water consumption rate and who had the same residence and workplace in one of six municipal water districts for 5 years before the serum sample (n = 1,074), predicted and observed median serum concentrations in 2005-2006 are 32.2 and 40.0 ppb, respectively (r s = 0.82). Conclusions: Serum PFOA concentrations predicted by linked exposure and ADME models correlated well with observed 2005-2006 human serum concentrations for C8 Health Project participants. These individualized retrospective exposure and serum estimates are being used in a variety of epidemiologic studies being conducted in this region.

Background: Benzene is a known occupational carcinogen associated with increased risk of hematologic cancers, but the relationships between quantity of passive benzene exposure through residential proximity to toxic release sites, duration of exposure, lag time from exposure to cancer development, and lymphoma risk remain unclear. Methods: We collected release data through the Environmental Protection Agency's Toxics Release Inventory (TRI) from 1989 to 2003, which included location of benzene release sites, years when release occurred, and amount of release. We also collected data on incident cases of non-Hodgkin lymphoma (NHL) from the Georgia Comprehensive Cancer Registry (GCCR) for the years 1999-2008. We constructed distance-decay surrogate exposure metrics and Poisson and negative binomial regression models of NHL incidence to quantify associations between passive exposure to benzene and NHL risk and examined the impact of amount, duration of exposure, and lag time on cancer development. Akaike's information criteria (AIC) were used to determine the scaling factors for benzene dispersion and exposure periods that best predicted NHL risk. Results: Using a range of scaling factors and exposure periods, we found that increased levels of passive benzene exposure were associated with higher risk of NHL. The best fitting model, with a scaling factor of 4 kilometers (km) and exposure period of 1989-1993, showed that higher exposure levels were associated with increased NHL risk (Level 4 (1.1-160 kilograms (kg)) vs. Level 1: risk ratio 1.56 [1.44-1.68], Level 5 (>160 kg) vs. Level 1: 1.60 [1.48-1.74]). Conclusions: Higher levels of passive benzene exposure are associated with increased NHL risk across various lag periods. Additional epidemiological studies are needed to refine these models and better quantify the expected total passive benzene exposure in areas surrounding release sites.

We conducted a cross-sectional study to assess the relationship between pesticide exposures and testosterone levels in 133 male Thai farmers. Urine and serum samples were collected concurrently from participants. Urine was analyzed for levels of specific and nonspecific metabolites of organophosphates (OPs), pyrethroids, select herbicides, and fungicides. Serum was analyzed for total and free testosterone. Linear regression analyses revealed significant negative relationships between total testosterone and the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) after controlling for covariates (eg, age, BMI, smoking status). Positive significant associations were found between some OP pesticides and total testosterone. Due to the small sample size and the observational nature of the study, future investigation is needed to confirm our results and to elucidate the biological mechanisms.