An assessment of agricultural pesticide use in Iran, 2012-2014.

BACKGROUND: This is the first published assessment on agricultural pesticide use in Iran with the aim to identify pesticide products with a potential of causing acute or chronic hazard to human health. It also establishes a baseline for future comparisons and for trend assessments. METHODS: The amounts of imported technical materials for formulation by local manufacturers as well as imported final product formulations were extracted from the registration data of the Plant Protection Organization of Iran in 2012-2014. The hazard indicators used were acute oral toxicity and chronic toxicity. For the latter, carcinogenicity, mutagenicity, and adverse effects on reproduction or development (CMR toxicity), and low Acceptable Daily Intake (ADI) were used. The comparative potential of the active ingredients of concern in terms of chronic toxicity was assessed using the average annual volume of their estimated use divided by their respective ADI, called chronic hazard potential (CHP) in the present text. The contribution of individual pesticides in different use categories to the total CHP of the user category, was also calculated, using the average annual volume of the active ingredients of all pesticides used during the period 2012-2014. RESULTS: On average about 14,000 tonnes of agriculture pesticides, expressed in active ingredients (AI), were annually used in Iran. Herbicides constituted the largest volume (43%), followed by insecticides and acaricides (37%) and fungicides (19%). 0.1% and 47% of the formulated products met the criteria of WHO Class Ib (highly hazardous) and Class II (moderately hazardous) products respectively. Aluminium phosphide and magnesium phosphide were identified as products of primary concern and chlorpyrifos, diazinon and paraquat as products of secondary concern, in terms of their acute human health hazard. No compound in carcinogenicity category 1A or 1B or germ cell mutagenicity/reproduction toxicity category 1A was identified. Six compounds (diazinon, chlorpyrifos, dichlorvos, metam sodium, paraquat and dimethoate) were identified as products with chronic hazard potential based on a low ADI. CONCLUSIONS: The assessment identified and prioritized agriculture pesticide used in Iran in terms of their acute and chronic hazard to human health for re-registration scheme recently established by PPO and for risk mitigation. It also set priority for research into development of alternative products and practices to minimize pesticide risks. Chronic hazard potential - amount of use adjusted with toxicity may serve as a useful point of reference for trend analysis also in the use of less hazardous agricultural pesticide products.

Occupational exposure to aluminum and its biomonitoring in perspective.

Exposure to aluminum at work is widespread, and people are exposed to several species of aluminum, which differ markedly as to the kinetics and toxicity. Especially welding of aluminum is widely applied and continuously expanding. Inhalation of fine particles of sparsely soluble aluminum results in the retention of deposited particles in the lungs. From the lungs, aluminum is released to the blood and distributed to bones and the brain, and excreted to urine. Soluble aluminum compounds are not accumulated in the lungs. Neurotoxicity is the critical effect of exposure to sparsely soluble aluminum compounds. Studies on workers exposed to aluminum welding fumes have revealed disturbances of cognitive processes, memory and concentration, and changes in mood and EEG. Early pulmonary effects have been observed among aluminum powder-production workers using high-resolution computed tomography. The primary objective of aluminum biomonitoring (BM) is to help prevent the formation of aluminum burden in the lungs and thereby to prevent harmful accumulation of aluminum in target organs. BM of aluminum can be effectively used for this purpose in the production/use of aluminum powders, aluminum welding, as well as plasma cutting, grinding, polishing and thermal spraying of aluminum. BM of aluminum may also be similarly useful in the smelting of aluminum and probably in the production of corundum. BM can help identify exposed individuals and roughly quantitate transient exposure but cannot predict health effects in the production/use of soluble aluminum salts. For urinary aluminum (U-Al) we propose an action limit of 3 µmol/L, corrected to a relative density of 1.021, in a sample collected preshift after two days without occupational exposure, and without use of aluminum-containing drugs. This value corresponds roughly to 2.3 µmol/g creatinine. Compliance with this limit is expected to protect the worker against the critical effect of aluminum in exposure to sparsely soluble aluminum dusts, the cognitive function of the central nervous system. For serum aluminum (S-Al), we do not propose an action limit because S-Al is less sensitive as an indicator of aluminum load.

Research needs for environmental health risk assessment.

Risk characterization comprises hazard characterization and exposure assessment. Hazard characterization may not be based on human data alone, as these data (1) are seldom available, (2) are quite insensitive in identifying the hazards, and (3) mostly lack reliable exposure-response information. Thus epidemiological information needs to be complemented with information from experimental animals and in vitro systems. These observations suffer from the necessity for species-to-species extrapolation, which is often based on weakly based generic default values. Default values may be replaced by chemical-specific uncertainty factors, but need to be applied cautiously and preferably in a predetermined framework with transparent guidance on what constitutes reliable evidence. Structure-activity relationships (SARs) are useful in setting priorities for hazard characterization and data generation, but seldom alone constitute a sufficient basis for quantitative hazard characterization. Little progress has been made in the assessment of the hazards from multiple simultaneous or successive exposures. Information on the exposure of the population whose risks are to be assessed relies predominantly on models of varying complexity. In the assessment of exposure to elements, speciation and bioavailability are important parameters for which the information often is limited.

Behavior of aluminum in aluminum welders and manufacturers of aluminum sulfate--impact on biological monitoring.

OBJECTIVES: The suitability of determining aluminum in serum or urine as a form of biological monitoring was critically assessed. METHODS: Airborne and internal aluminum exposure was assessed for 12 aluminum welders in a shipyard and 5 manufacturers of aluminum sulfate. Particles were characterized with X-ray diffraction and scanning electron microscopy. Aluminum in air and biological samples was analyzed using electrothermal atomic absorption spectrometry. Basic toxicokinetic features were inferred from the data. RESULTS: The mean 8-hour time-weighted average concentration of aluminum was 1.1 (range 0.008-6.1) mg/m(3) for the shipyard and 0.13 (range 0.02-0.5) mg/m(3) for the aluminum sulfate plant. Welding fume contained aluminum oxide particles <0.1 microm in diameter and their agglomerates, whereas bauxite and aluminum sulfate particles ranged from 1 to 10 microm in diameter. The shipyard welders' mean postshift serum and urinary concentrations of aluminum (S-Al and U-Al, respectively) were 0.22 and 3.4 micromol/l, respectively, and the aluminum sulfate workers' corresponding values were 0.13 and 0.58 micromol/l. Between two shifts, the welders' S-Al concentration decreased by about 50% (P<0.01), but their U-Al concentration did not change (P=0.64). No corresponding temporal changes occurred among the aluminum sulfate workers. After aluminum welding at the shipyard had ceased, the median S-Al concentration decreased by about 50% (P=0.007) within a year, but there was no change (P=0.75) in the corresponding U-Al concentration. CONCLUSIONS: About 1% of aluminum in welding fume appears to be rapidly absorbed from the lungs, whereas an undetermined fraction is retained and forms a lung burden. A higher fractional absorption of aluminum seems possible for aluminum sulfate workers without evidence of a lung burden. After rapid absorption, aluminum is slowly mobilized from the lung burden and dominates the S-Al and U-Al concentrations of aluminum welders. For kinetic reasons, S-Al or U-Al concentrations cannot be used to estimate the accumulation of aluminum in the target organs of toxicity. However, using U-Al analysis to monitor aluminum welders' lung burden seems practical.

Toxicokinetics of methyl tert-butyl ether (MTBE) and tert-amyl methyl ether (TAME) in humans, and implications to their biological monitoring.

Healthy male volunteers were exposed via inhalation to gasoline oxygenates methyl tert-butyl ether (MTBE) or tert-amyl methyl ether (TAME). The 4-hr exposures were carried out in a dynamic chamber at 25 and 75 ppm for MTBE and at 15 and 50 ppm for TAME. The overall mean pulmonary retention of MTBE was 43 +/- 2.6%; the corresponding mean for TAME was 51 +/- 3.9%. Approximately 52% of the absorbed dose of MTBE was exhaled within 44 hr following the exposure; for TAME, the corresponding figure was 30%. MTBE and TAME in blood and exhaled air reached their highest concentrations at the end of exposure, whereas the concentrations of the metabolites tert-butanol (TBA) and tert-amyl alcohol (TAA) concentrations were highest 0.5-1 hr after the exposure and then declined slowly. Two consecutive half-times were observed for the disappearance of MTBE and TAME from blood and exhaled air. The half-times for MTBE in blood were about 1.7 and 3.8 hr and those for TAME 1.2 and 4.9 hr. For TAA, a single half-time of about 6 hr best described the disappearance from blood and exhaled air; for TBA, the disappearance was slow and seemed to follow zero-order kinetics for 24 hr. In urine, maximal concentrations of MTBE and TAME were observed toward the end of exposure or slightly (< or = 1 hr) after the exposure and showed half-times of about 4 hr and 8 hr, respectively. Urinary concentrations of TAA followed first-order kinetics with a half-time of about 8 hr, whereas the disappearance of TBA was slower and showed zero-order kinetics at concentrations above approx. 10 micro mol/L. Approximately 0.2% of the inhaled dose of MTBE and 0.1% of the dose of TAME was excreted unchanged in urine, whereas the urinary excretion of free TBA and TAA was 1.2% and 0.3% within 48 hr. The blood/air and oil/blood partition coefficients, determined in vitro, were 20 and 14 for MTBE and 20 and 37 for TAME. By intrapolation from the two experimental exposure concentrations, biomonitoring action limits corresponding to an 8-hr time-weighted average (TWA) exposure of 50 ppm was estimated to be 20 micro mol/L for post-shift urinary MTBE, 1 mu mol/L for exhaled air MTBE in a post-shift sample, and 30 micro mol/L for urinary TBA in a next-morning specimen. For TAME and TAA, concentrations corresponding to an 8-hr TWA exposure at 20 ppm were estimated to be 6 micro mol/L (TAME in post-shift urine), 0.2 micro mol/L (TAME in post-shift exhaled air), and 3 micro mol/L (TAA in next morning urine).

Zero exposure--a goal for environmental and occupational health?

Humans live on chemicals, and no exposure to any chemicals is incompatible with life. Chemicals produced by different organisms are in no basic way different from the man-made chemicals, and often chemicals are produced by both. Natural chemicals include the most potent acutely toxic chemicals known, and also include very potent mutagens and human carcinogens. Thus the fact that a chemical is 'natural' does not mean that it is any safer than a man-made chemical, and the fact that a chemical is man-made does not make it any more harmful than 'natural' chemicals. Exposure to chemicals varies widely, to a large variety of chemicals people are exposed from the environment, via drinking water, food and inhaled air and exposure e.g. at the work-place is only quantitatively different from the exposure of the general public. Zero exposure is meaningless without an operational definition. It is a major challenge to the society to determine what is the safe exposure level to different chemicals, and for chemicals for which no exposure level is safe, to define the acceptable risk, and in both cases, make sure that the exposure limits thus determined are complied with.