In 2000, the Agency for Toxic Substances and Disease Registry (ATSDR; Atlanta, GA, USA) investigated lung disease in those exposed to the tremolite-contaminated vermiculite mine in Libby, MT, USA. Previously unreported spirometric results are presented here in relation to exposure and radiographic findings. 4,524 study participants were assigned to one of seven mutually exclusive exposure categories. Associations among radiographic findings, spirometric results and exposure were investigated, along with the effect of a reduction in exposure potential when production was moved to a wet process mill in the mid 1970s. Spirometry data for the total population by smoking status and age were within the normal range. Prevalence of pleural plaque increased with age, but was lowest in the environmentally exposed group (0.42–12.74%) and greatest in the W.R. Grace & Co. mineworkers (20–45.68%). For males, there was a significant (4.5%) effect of pleural plaques on forced vital capacity. For W.R. Grace & Co. workers and household contacts, a reduction in plaque (0.11 versus 1.64%) and in diffuse pleural thickening or costophrenic angle obliteration (1.94 and 0.13%) was noted for those exposed after 1976. These analyses do not support a clinically important reduction in spirometry of this cohort. The 1976 reductions in exposure have led to decrease in radiographic changes.

The RespiConTMsampler is a multistage virtual impactor that simultaneously collects the ISO/CEN/ACGIH size fractions of inhalable, thoracic, and respirable particulate matter. The field performance of the device for measurement of industrial wood processing dust was evaluated against reference size-selective samplers: the IOM sampler (inhalable dust), the GK 2.69 cyclone (thoracic dust), and the SKC aluminum cyclone (respirable dust). Seventy-one sets of area samples were collected from 10 wood processing plants, with the samplers mounted either in the free-field or on a two-dimensional “bluff body.” The geometric mean (range) dust levels across all plants measured by the reference samplers were: inhalable, 1.35 mg/ m3(0.11–11.06); thoracic, 0.31 mg/m3(0.05–1.38); and respirable, 0.10 mg/m3(0.02–0.54). In comparing the RespiCon with the reference samplers, there was no significant difference between sampling in the free-field versus bluff-body modes. For inhalable dust, there was no significant difference between the RespiCon and the IOM sampler after applying a correction factor of 1.5× to the extrathoracic data obtained from the RespiCon. Without the correction factor, the RespiCon undersample inhalable dust by an average of 23%. For thoracic dust, the RespiCon was shown to oversample the extrathoracic dust fraction resulting in an overall error of 48%. A simple correction based on the inhalable and thoracic dust levels reported by the RespiCon is proposed. For respirable dust, there was a significant difference between the RespiCon and the SKC cyclone, but the data were equivocal due to imprecision in measurement of the low respirable dust concentrations encountered and the likelihood of bias in the reference sampler. Overall, the RespiCon sampler appears to be a suitable size-selective sampling device for industrial wood processing dust, although adjustments should be made to the inhalable and thoracic dust results.

They are still A- botThere are less destructive viruses around – there is no doubt about it. Where are the Blasters and Slammers? Dr Gene Schultz believes that they have been reborn as bots.Malware writers are shifting their focus from unleashing massive, destructive viruses to harvesting thousands of bots. Botnets are stealth and sneaky, trying to avoid detection – while old school viruses like Blaster were loud and ubiquitous. Bots work quietly while the viruses of old wreaked unmissable havoc across thousands of computers internationally. And some anti-virus tools are sometimes useless in recognising botnets. Botnets are much more widespread than people know – the stealth way in which they operate makes them hard to detect. The switch from viruses and worms is likely due to the variety of ways that bots can make money for zombie masters. Botnets can be sold, used to send spam, for Dos attacks and extortion. Schultz also explores other reasons for why there are less mass worms as follows: •More companies use anti-virus software.•There are fewer vulnerabilities for viruses to exploit.•Boredom has demotivated virus and worm writers.•Worm and virus writers are scared of the repercussions.•Worms and viruses target more niche systems were mass spreading is impossible.There is a new trend in malware and organizations have to adapt to fight it.Although many new worms and viruses surface every week, they are becoming less widespread than those in previous years. In contrast, bots and botnets are becoming more prolific and troublesome; botnets consisting of hundreds of thousands of bots or even more are not uncommon. Bot writers and botnet operators have numerous motives for engaging in their sordid activity, but the desire to make money has become by far the chief motivator. Meanwhile, the nature of current worms and viruses is also changing considerably—a growing number of them uses instant messaging (IM) to replicate, and worms and viruses that target handheld computing devices are also becoming more prevalent. Bots and botnets pose very elevated levels of risk, risk that needs to be controlled through a variety of security countermeasures.

Results of isocyanate challenge tests performed on 63 workers referred with a diagnosis of probable isocyanate asthma between 1974 and 1988 were reviewed. Thirty (48 percent) had an acute episode of asthma with a greater than 20 percent decline in FEV1 following subirritant exposure to isocyanates. No difference in the frequency or type of respiratory complaints between isocyanate reactors and nonreactors was found. No differences in lung function results were present when comparing smoking and ex-smoking reactors and nonreactors. In never-smokers with complaints consistent with isocyanate-induced asthma, the presence of obstructive lung disease increased the likelihood that isocyanate-induced asthma was present. Bronchial responsiveness to methacholine occurred in nearly all isocyanate reactors but predicted isocyanate-induced asthma in only 68 percent of the workers. In nearly all cases of challenge-confirmed toluene diisocyanate (TDI)-induced asthma, a 15-min exposure to 20 ppb of the commercial TDI mixture (80:20 2,4:2,6) provoked asthma. Conversely, in the absence of an asthmatic response following exposure to this dose for this duration, a second exposure at this concentration for a longer time would be reasonable to confirm the absence of isocyanate-induced asthma. Among workers employed in the production of polyurethane foam and confirmed to have TDI-induced asthma by inhalation challenge to the different TDI isomers, there appeared to be increased airway reactivity to the 2,6 isomer. This may have relevance to the frequency and intensity of respiratory symptoms that workers with TDI-induced asthma develop in differing industrial settings.

The effects of exposure to environmental tobacco smoke on pulmonary function were assessed in 21 subjects with asthma who claimed respiratory complaints (cough, shortness of breath, and chest tightness) on previous exposure to cigarette smoke. Exposure to mechanically produced tobacco smoke was performed in a static inhalation chamber for two-hour intervals at two distinct smoke levels (as measured by carbon monoxide, nicotine, and particulate levels). Seven of the 21 smoke-challenged subjects experienced a significant (greater than 20%) decline in FEV1 during passive exposure to tobacco smoke. One of these seven subjects was nonatopic, whereas a second subject had a negative response to methacholine challenge. The smoke-challenge responses were reproducible in all seven reactive subjects. Increasing concentrations of tobacco smoke failed to elicit pulmonary changes in previously challenged, unreactive or "smoke-tolerant" subjects. There was no association between a positive smoke challenge and the presence of serum IgE antibodies and/or a positive immediate wheal-and-flare skin test to a tobacco leaf extract. Collectively, these studies document a significant decline in pulmonary function in a substantial percentage (33%) of a population of "smoke-sensitive" subjects with asthma exposed to environmental tobacco smoke. The data also dissociate this effect from tobacco-leaf hypersensitivity.

Chlorine gas, spreading from a train derailment, caused the deaths of 8 persons and the hospitalization of 23 with sublethal respiratory injuries. Twenty-five others had at least one sign of lower respiratory abnormality but were not hospitalized. One hundred thirteen who were examined for gas effects in the forty-eight hours after exposure, including 20 of 23 of those hospitalized and 21 of 25 of those not hospitalized but with respiratory abnormality, participated in follow-up studies. Probability of admission to hospital was related to distance from the spill, but by 3 wk after exposure there was no detectable difference in lung function relating to distance or apparent severity of injury. In 60 adults tested multiple times over the following 6 yr, longitudinal change in lung function showed expected differences related to smoking but none related to distance or severity of injury. The average annual change in FEV was -34 ml/yr in current smokers and -18 ml/yr in ex and never-smokers. The lack of a discernible chlorine effect in this cohort accords with the findings in most previous studies. Without pre-exposure measurements, a single, lasting reduction in lung function cannot be excluded, but there is no evidence for a persisting abnormal rate of decline.

An analysis of variability within individuals was conducted for FEV1, obtained from subjects employed in the cottonseed industry. Individual SDs ranged from .020 to .428 L. The within-subject SD of the preshift-postshift difference ranged from .014 to .302 L. When within-subject variability of FEV1 was analyzed in relation to symptoms, smoking history, and shift, the only statistical difference occurred in the 14 bronchitic subjects (.141 L) relative to the 179 without bronchitis (.099 L), and the three subjects with byssinosis (.192 L) relative to those without symptoms (.102 L). Changes over the working shift were significantly different for evening relative to morning and night shifts, even though there was no significant difference in smoking status, symptoms, exposure, race, age, years employed in the mill, and work area. In addition, baseline measurements were not significantly related to shift. Therefore, the effect of individual variability, symptoms, and shift should be considered if an accurate classification of reactors based on change in FEV1 across the shift is to be obtained.

This presentation summarizes our experience in three cross-sectional studies of respiratory health in cottonseed crushing mills. These studies were done in 1975, 1977, and 1978. Three mills were visited on all three occasions, another twice, and another once. In the course of these studies, health data were collected on a total of 444 subjects in the five mills.

Four hundred and eighty-six textile workers in three cotton mills and one wool/synthetic mill were studied for symptoms and functional effects of workroom exposure to dust. Byssinosis was found in 5.7% of 386 cotton workers, with an apparent threshold level of 0.5 mg cotton dust/m3 of air. Mean post-shift functional declines were greater in workers exposed to greater than or equal to 0.2 mg/m3. Workers with byssinosis were unequally distributed, however, with respect to job category and mill; and these variables, rather than current dust exposure levels, accounted for the observed distribution of byssinosis prevalence rates. Variation in biological potency of different samples of cotton dust could be responsible for 'mill effect', the residual variation in response rates by mill after controlling for variation due to dust exposure. A number of other potential influencing variables that are likely to be distributed unequally by mill should also be considered. Mill effect should be assessed in large-scale studies of byssinosis, most of which have analysed biological response rates by combining mill and other variables to examine first-order effects of dust dosage. In such analyses, much of the observed variability may be due to factors other than dust dosage.