On 18 farms for rose culture in greenhouses in The Netherlands, dermal exposure of hands and forearms to abamectin (avermectin B1), dodemorph (4-cyclododecyl-2,6-dimethylmorpholinium acetate) and bupirimate (5-butyl-2-(ethylamino)-6-methyl-4-pyrimidinyl dimethylsulphate) was measured during crop activities. Dermal exposure during cutting (75 workers) amounted to 13 micrograms/h, 1.8 mg/h, and 2.2 mg/h for abamectin, dodemorph and bupirimate, respectively. Dermal exposure to abamectin and dodemorph during sorting (21 workers) and bundling (30 workers) was comparable with that during cutting. From the dependence of dermal exposure on the amount of dislodgeable foliar residue (DFR) a transfer factor was estimated to be 1,200, 4,550, and 2,400 cm2/h for abamectin, dodemorph and bupirimate, respectively. For sorting and bundling these factors were of the same order of magnitude. The results suggested that work rate was also a determinant of dermal exposure. The within-farm variance of dermal exposure during cutting appeared to account for approximately 30% of the unexplained part of the variation remaining after regression on DFR and application technique. The final unexplained part in the variation of dermal exposure during cutting was amongst others due to the variation between the different farms in which the measurements were performed. A health risk evaluation of the observed levels of dermal exposure after re-entry of greenhouses led to the conclusion that a health hazard may exist, especially after application of high rates of relatively toxic pesticides which easily penetrate the skin.

The mechanisms of inactivation of aerosolized bacteriophage phiX174 in atmospheres containing ozone, cyclohexene, or ozonized cyclohexene were studied by using 32P-labelled phage. The inactivation of the aerosolized phage in clear air or in air containing cyclohexene is due to damage of the protein coat since the deoxyribonucleic acid (DNA) extracted from the inactivated phage retains its biological activity. Inactivation of the phage in air containing ozonized cyclohexene is due both to protein and DNA damage. Sucrose gradient analysis shows that aerosolized inactivated phiX174 releases unbroken DNA. In contrast, the DNA from phage phiX174 inactivated by ozonized cyclohexene is broken. The inactivation of aerosolized phage phiX174-DNA was studied in the same atmospheres using 32P-labelled DNA. phiX174-DNA aerosolized in clear air or air containing cyclohexene at 75% r.h. is inactivated by a factor of 2 in 30 min. The inactivated DNA is broken. Ozone as well as ozonized cyclohexene inactivates KNA very fast causing breaks in the molecule. This is in contrast with the intact bacteriophage in which ozone does not produce breaks in the DNA.

In the absence of ozone the OAF concentration was always low. In the presence of ozone the OAF concentration was dependent on wind direction. At the selected microthread exposure sites air from areas with high traffic intensity contributed more to OAF production than air from industrial areas. OAF production is probably related to the nature of hydrocarbons in the air.

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The inactivation of aerosolized Escherichia coli by ozone, cyclohexene, and ozonized cyclohexene was studied. The parameters for damage were loss of reproduction and introduction of breaks in the deoxyribonucleic acid (DNA). Aerosolization of E. coli in clean air at 80% relative humidity or in air containing either ozone or cyclohexene hardly affected survival; however, some breaks per DNA molecule were induced, as shown by sucrose gradient sedimentation of the DNA. Aerosolization of E. coli in air containing ozonized cyclohexene at 80% relative humidity decreased the survival by a factor of 103 or more after 1 h of exposure and induced many breaks in the DNA.

Respiratory exposure and dermal exposure of the hands and forearms to the pesticides chlorothalonil, thiophanate-methyl, thiram, and zineb during application and during crop activities have been measured on 18 farms for carnation culture in glass-covered greenhouses in the Netherlands. Farms were selected according to a "worst case" strategy with regard to dermal exposure during cutting of flowers. For 94 workers, the geometric mean dermal exposure rate during cutting (measured on long-sleeved cotton glove monitors) was 10.1 mg/hr (active ingredient per unit of actual working time) and during sorting/bundling of these flowers by 35 workers the dermal exposure rate was 7.3 mg/hr. The average concentration in air as measured by personal air sampling during cutting after a pesticide had been dusted was 0.07 mg/m3. For the same area, spraying a pesticide exposed the applicator to a dermal exposure seven times higher than dusting. However, during dusting respiratory exposure was higher. Generally, overall exposure is higher during re-entry activities than during application. From the observed levels of dermal exposure during harvesting (re-entry) and from toxicity data, health risk occurs after application of pesticides that are relatively toxic and show relatively good skin-penetrating properties at relatively high application rates. The respiratory exposure to dusted pesticides after re-entry is about as high as during application of these pesticides and may in some situations also result in health risks. Training and education of greenhouse workers on (personal) hygiene and use of protective gloves are advocated in order to reduce exposure.

Methyl n-butyl ketone (MBK) was considered rather harmless until an outbreak of peripheral neuropathy occurred in 1973 among workers exposed to MBK. MBK easily penetrates the skin; pulmonary retention is approximately 80-85% in man. Distribution is widespread with highest levels in blood and liver; MBK also reaches the fetal tissues. MBK metabolism probably depends on the route of exposure, and is very similar to that of n-hexane. The critical organ is the nervous system. These effects find expression as peripheral neuropathy, with potential for serious effects of the central nervous system. From the viewpoint of neurotoxicity, 2,5-hexanedione is the most important metabolite. The neurotoxicity is potentiated by several compounds, while MBK itself potentiates the toxicity of other chemicals. From animal experiments, a no-adverse-effect level (NAEL) could not be established. Peripheral neuropathy may develop in workers exposed to only a few ppm of MBK. The difference in the Occupational Exposure Limits for MBK and n-hexane, as established by several organizations, is questioned in view of the neurotoxic effects of these substances.

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