The relationship between alcohol consumption and the desire to own a firearm: an empirical study on citizens of São Paulo city, Brazil.

OBJECTIVE: The main objective of this study was to investigate the association between alcohol consumption (use and bingeing) and the desire to own a firearm for protection. STUDY DESIGN: We used data from three random cross-sectional victimisation surveys conducted in São Paulo city, Brazil, in 2003, 2008 and 2013 with people aged ≥16 years. METHODS: We performed tests for equality of proportions. Our analysis was performed separately for each victimisation survey to check the robustness of the results. We also used probit models, estimated by the maximum likelihood method, to analyse the relationship between desire to own a firearm and alcohol consumption, controlling for many other variables. RESULTS: In 2013, although only 1.5% of the population surveyed reported living in a household with a firearm, 15.7% report that they would possess a firearm if they could, and 13.0% believed they would be safer/more protected from violence if they had a firearm. The desire to own a firearm is higher among people who consume alcoholic beverages than among those who do not and is higher as alcohol binge frequency increases. CONCLUSION: In São Paulo city, alcohol consumption and binge drinking are positively associated with the desire to own a firearm.

Intimate partner violence perpetration, standard and gendered STI/HIV risk behaviour, and STI/HIV diagnosis among a clinic-based sample of men.

BACKGROUND: The estimated one in three women worldwide victimized by intimate partner violence (IPV) consistently demonstrate elevated STI/HIV prevalence, with their abusive male partners' risky sexual behaviours and subsequent infection increasingly implicated. To date, little empirical data exist to characterise the nature of men's sexual risk as it relates to both their violence perpetration, and STI/HIV infection. METHODS: Data from a cross-sectional survey of men ages 18-35 recruited from three community-based health clinics in an urban metropolitan area of the northeastern US (n = 1585) were analysed to estimate the prevalence of IPV perpetration and associations of such violent behaviour with both standard (eg, anal sex, injection drug use) and gendered (eg, coercive condom practices, sexual infidelity, transactional sex with a female partner) forms of sexual-risk behaviour, and self-reported STI/HIV diagnosis. RESULTS: Approximately one-third of participants (32.7%) reported perpetrating physical or sexual violence against a female intimate partner in their lifetime; one in eight (12.4%) participants self-reported a history of STI/HIV diagnosis. Men's IPV perpetration was associated with both standard and gendered STI/HIV risk behaviours, and to STI/HIV diagnosis (OR 4.85, 95% CI 3.54 to 6.66). The association of men's IPV perpetration with STI/HIV diagnosis was partially attenuated (adjusted odds ratio (AOR) 2.55, 95% CI 1.77 to 3.67) in the multivariate model, and a subset of gendered sexual-risk behaviours were found to be independently associated with STI/HIV diagnosis-for example, coercive condom practices (AOR 1.67, 95% CI 1.04 to 2.69), sexual infidelity (AOR 2.46, 95% CI 1.65 to 3.68), and transactional sex with a female partner (AOR 2.03, 95% CI 1.36 to 3.04). CONCLUSIONS: Men's perpetration of physical and sexual violence against intimate partners is common among this population. Abusive men are at increased risk for STI/HIV, with gendered forms of sexual-risk behaviour partially responsible for this association. Thus, such men likely pose an elevated infection risk to their female partners. Findings indicate the need for interwoven sexual health promotion and violence prevention efforts targeted to men; critical to such efforts may be reduction in gendered sexual-risk behaviours and modification of norms of masculinity that likely promote both sexual risk and violence.

Recent psychopathology, suicidal thoughts and suicide attempts in households with and without firearms: findings from the National Comorbidity Study Replication.

OBJECTIVE: To assess the relationship between firearm ownership and possible psychiatric confounders of the firearm-suicide relationship. METHODS: Multivariate logistic regression was used to estimate the association between living in a home with firearms and 12-month occurrence of major Diagnostic and statistical manual of mental disorders (DSM)-IV disorders and suicidal behaviour among respondents to the National Comorbidity Survey Replication, a household survey of 9282 adults aged 18+. Analyses controlled for sociodemographic characteristics including age, sex, race/ethnicity, educational attainment and poverty. RESULTS: Approximately one in three Americans reported living in a home with firearms. People living in a home with firearms were no more or less likely than people in homes without firearms to have recent (past year) anxiety disorders (OR = 1.0, 95% CI 0.8 to 1.2), mood disorders (OR = 0.9, 95% CI 0.7 to 1.1) or substance dependence and/or abuse (OR = 0.9, 95% CI 0.6 to 1.3). Past year suicidal ideation (OR = 0.8, 95% CI 0.5 to 1.3) and suicide planning (OR = 0.5, 95% CI 0.2 to 1.4) were also not associated with living in households with firearms. Having made a suicide attempt over the previous year was the only outcome more common among participants reporting that they currently lived in a home without [corrected] firearms. CONCLUSIONS: The previously reported association between household firearm ownership and heightened risk of suicide is not explained by a higher risk of psychopathology among gun-owning families. As there are Americans with suicidal ideation and/or significant and recent psychiatric disorders currently living in homes with firearms, future work should focus on understanding the impediments to effectively communicating the suicide risk associated with household firearms.

Asbestos inhalation induces reactive nitrogen species and nitrotyrosine formation in the lungs and pleura of the rat.

To determine whether asbestos inhalation induces the formation of reactive nitrogen species, three groups of rats were exposed intermittently over 2 wk to either filtered room air (sham-exposed) or to chrysotile or crocidolite asbestos fibers. The rats were killed at 1 or 6 wk after exposure. At 1 wk, significantly greater numbers of alveolar and pleural macrophages from asbestos-exposed rats than from sham-exposed rats demonstrated inducible nitric oxide synthase protein immunoreactivity. Alveolar macrophages from asbestos-exposed rats also generated significantly greater nitrite formation than did macrophages from sham-exposed rats. Strong immunoreactivity for nitrotyrosine, a marker of peroxynitrite formation, was evident in lungs from chrysotile- and crocidolite-exposed rats at 1 and 6 wk. Staining was most evident at alveolar duct bifurcations and within bronchiolar epithelium, alveolar macrophages, and the visceral and parietal pleural mesothelium. Lungs from sham-exposed rats demonstrated minimal immunoreactivity for nitrotyrosine. Significantly greater quantities of nitrotyrosine were detected by ELISA in lung extracts from asbestos-exposed rats than from sham-exposed rats. These findings suggest that asbestos inhalation can induce inducible nitric oxide synthase activation and peroxynitrite formation in vivo, and provide evidence of a possible alternative mechanism of asbestos-induced injury to that thought to be induced by Fenton reactions.

Ambient particulate matter causes activation of the c-jun kinase/stress-activated protein kinase cascade and DNA synthesis in lung epithelial cells.

Numerous epidemiological studies have demonstrated a positive association between ambient air pollution and adverse health effects including respiratory morbidity, asthma, and lung cancer. It has been suggested in some experimental studies that airborne particulate matter (PM) can produce inflammatory effects, but nothing is known about the possible proliferative and carcinogenic effects of these particles on cells of the lung. We show here that exposure of pulmonary epithelial cells, a cell type affected in acute lung injury, asthma, and lung carcinomas, to nontoxic concentrations of PM in vitro results in increases in c-jun kinase activity, levels of phosphorylated cJun immunoreactive protein, and transcriptional activation of activator protein-1-dependent gene expression. These changes are accompanied by elevations in numbers of cells incorporating 5'-bromodeoxyuridine, a marker of unscheduled DNA synthesis and/or cell proliferation. Data here are the first to demonstrate that interaction of ambient PM with target cells of the lung initiates a cell signaling cascade related causally to aberrant cell proliferation and carcinogenesis.

Mechanisms of asbestos-induced nitric oxide production by rat alveolar macrophages in inhalation and in vitro models.

To evaluate the contribution of reactive nitrogen species to inflammation by asbestos, Fischer 344 rats were exposed to crocidolite or chrysotile asbestos by inhalation to determine whether increases occurred in nitric oxide (NO.) metabolites from alveolar macrophages (AMs). AMs from animals inhaling asbestos showed significant elevations (p < .05) in nitrite/nitrate levels which were ameliorated by NG-monomethyl-L-arginine (NMMA), an inhibitor of inducible nitric oxide synthase (iNOS) activity. Temporal patterns of NO. generation from AMs correlated with neutrophil influx in bronchoalveolar lavage samples after asbestos inhalation or bleomycin instillation, another model of pulmonary fibrosis. To determine the molecular mechanisms and specificity of iNOS promoter activation by asbestos, RAW 264.7 cells, a murine macrophage-like line, and AMs isolated from control rats were exposed to crocidolite asbestos in vitro. These cells showed increases in steady-state levels of iNOS mRNA in response to asbestos and more dramatic increases in both iNOS mRNA and immunoreactive protein after addition of lipopolysaccharide (LPS). After transfection of an iNOS promoter/luciferase reporter construct, RAW 264.7 cells exposed to LPS, crocidolite asbestos and its nonfibrous analog, riebeckite, revealed increases in luciferase activity whereas cristobalite silica had no effects. Studies suggest that NO. generation may be important in cell injury and inflammation by asbestos.

Firearm prevalence and social capital.

PURPOSE: Previous studies have shown a correlation between measures of social capital and morbidity, mortality, and violent crime. This article examines the association across U.S. states between social capital (as measured by mutual trust and civic engagement) and firearm availability. METHODS: The analysis uses OLS to determine degrees of association across U.S. states. Measures of mutual trust come from responses to questions on the U.S. General Social Survey that "you can't be too careful in dealing with people," and most people "would try to take advantage of you." Measures of formal civic engagement come from responses to Lifestyle Survey questions concerning times volunteered, club meetings attended, community projects worked on, and church services attended. Informal civic engagement measures come from responses to number of times bowled, played cards, entertained at home, and gave or attended dinner parties, and number of greeting cards sent. The Lifestyle Survey also asked whether respondent believed whether "most people are honest." The percentage of suicides from firearms, and the average percentage of suicides and homicides from firearms, are used as proxies for state firearm ownership rates. Control variables are the degree of urbanization, the rates of poverty, and the percentage of nonwhites in the state. RESULTS: Across the U.S. states, higher levels of firearm ownership are associated with significantly lower levels of mutual trust and civic engagement. CONCLUSION: While the analysis cannot show causation, states with heavily armed civilians are also states with low levels of social capital.

Pleural macrophage recruitment and activation in asbestos-induced pleural injury.

The pathogenesis of asbestos-induced pleural fibrosis is poorly understood. Moreover, there has been a long-standing controversy regarding the relative potential of different commercial types of asbestos to cause pleural disease. We postulated that inhaled asbestos fibers translocate to the pleural space where they stimulate the recruitment and activation of pleural macrophages. To test this hypothesis, and to determine whether there are differences between inhaled amphibole and serpentine asbestos, Fischer 344 rats were exposed by intermittent inhalation (6 hr/day for 5 days/week over 2 weeks) to either National Institute of Environmental Health Sciences (NIEHS) crocidolite (average concentration 7.55 mg/m3) or NIEHS chrysotile fibers (average concentration 8.51 mg/m3). Comparisons were made with sham-exposed rats. The rats were sacrificed at 1 and 6 weeks after the cessation of exposure. More pleural macrophages were recovered at 1 and 6 weeks after crocidolite and chrysotile exposure than after sham exposure. Small numbers of crocidolite fibers (approximately 1 per 4000 cells) were detected in the pleural cell pellet of one crocidolite-exposed rat by scanning electron microscopy. Pleural macrophage supernatants were assayed for production of nitric oxide (NO) (by the Griess reaction) and tumor necrosis factor alpha (TNF-alpha) (by an enzyme-linked immunosorbent assay method). Significantly greater amounts of NO as well as TNF-alpha were generated by pleural macrophages at 1 and 6 weeks after either crocidolite or chrysotile inhalation than after sham exposure. Conceivably, translocation of asbestos fibers to the pleural space may provide a stimulus for persistent pleural space inflammation, cytokine production, and the generation of toxic oxygen and nitrogen radicals. Enhanced cytokine secretion within the pleural space may in turn upregulate adhesion molecule expression and the synthesis of extracellular matrix constituents by pleural mesothelial cells. Thus, our findings may have significance for the development of asbestos-induced pleural injury.

The second best in statistics.

When estimating a parameter, it may not be possible to remove all sources of bias. Yet a priori we do not know whether eliminating some sources will improve or worsen the estimate.

Radiographic abnormalities in Vermont granite workers exposed to low levels of granite dust.

The issue of whether low levels of granite dust exposure lead to radiographic abnormalities after a lifetime of exposure has not been settled. In 1983, we carried out a radiographic survey of the Vermont granite industry, consisting of quarry and stone shed workers who had been exposed to the low dust levels prevailing in the industry since 1938 to 1940. Films were read by three "B" readers, using the ILO classification system, which requires the identification of both rounded and irregular opacities, as well as combinations of both. X-ray films were taken of 972 workers, out of a total work force of approximately 1,400. Of these films, 28 (3 percent) were interpreted by either two or three of the three readers as showing abnormalities consistent with pneumoconiosis. Only seven films (or 0.7 percent of the entire cohort) showed nodular or rounded opacities of the type typically seen in uncomplicated silicosis. The remainder of the abnormal x-ray films showed irregular opacities, largely in the lower lung zones, which are of uncertain significance, but may be related to heavy cigarette smoking and aging, and possibly dust inhalation. In addition, total gravimetric dust concentrations in the workplace were measured; 417 respirable-size mass samples showed concentrations of 601 micrograms/cu m +/- 368 micrograms/cu m. Using previously published estimates of 10 percent quartz in granite dust, the average quartz concentration was 60 micrograms/cu m. Twelve percent of the samples exceeded 100 micrograms/cu m, the current OSHA standard for quartz. We conclude that control of quartz exposure in the Vermont granite industry to levels which are on average less than the current OSHA standard has essentially eliminated definite radiographic changes of silicosis. The significance of the irregular opacities in the lower lung zones seen on a majority of the 28 x-ray films judged to be abnormal is not clear.

Body height and hip fracture: a cohort study of 90,000 women.

BACKGROUND: Hip fractures are a major public health problem. Recent studies have noted a connection between body height and hip fracture. METHODS: We investigated the relationship between body height and hip fracture using a prospective cohort of over 92,000 American, predominantly white, female nurses who were followed for 10 years, from June 1980 to June 1990. The women, participants in the Nurses Health Study, were aged 35-59 in 1980. RESULTS: Women 5'8" or taller were more than twice as likely as women under 5'2" to sustain a hip fracture, after accounting for age, body mass index, cigarette smoking and alcohol consumption (multivariate relative risk 2.40, 95% confidence interval: 1.43-4.02; P for trend < 0.0001). CONCLUSION: Height appears to be an important independent risk factor for hip fracture among American women. Height should be included as a confounder in studies of hip fracture, and taller, elderly women should be advised to consider preventive measures.

High injury rates among female army trainees: a function of gender?

BACKGROUND: Studies suggest that women are at greater risk than men for sports and training injuries. This study investigated the association between gender and risk of exercise-related injuries among Army basic trainees while controlling for physical fitness and demographics. METHODS: Eight hundred and sixty-one trainees were followed during their 8-week basic training course. Demographic characteristics, body composition, and physical fitness were measured at the beginning of training. Physical fitness measures were taken again at the end of training. Multivariate logistic regression analysis was used to evaluate the association between gender and risk of injury while controlling for potential confounders. RESULTS: Women experienced twice as many injuries as men (relative risk [RR] = 2.1, 1.78-2.5) and experienced serious time-loss injuries almost 2.5 times more often than men (RR = 2.4, 1. 92-3.05). Women entered training at significantly lower levels of physical fitness than men, but made much greater improvements in fitness over the training period.In multivariate analyses, where demographics, body composition, and initial physical fitness were controlled, female gender was no longer a significant predictor of injuries (RR = 1.14, 0.48-2.72). Physical fitness, particularly aerobic fitness, remained significant. CONCLUSIONS: The key risk factor for training injuries appears to be physical fitness, particularly cardiovascular fitness. The significant improvement in endurance attained by women suggests that women enter training less physically fit relative to their own fitness potential, as well as to men. Remedial training for less fit soldiers is likely to reduce injuries and decrease the gender differential in risk of injuries.

Precursors of lethal violence: a death row sample.

A qualitative methodology based on the standards of criminal defense investigation was used to analyze the social and family histories of 16 men sentenced to death in California. Using a multisource cross-validation methodology, we assessed patterns of impairment, injury and deficit at each of four ecological levels: family, individual, community and social institutions. Investigation documented consistent and pervasive patterns of serious impairment, injury and deficit across the cases and levels. The men share numerous risk factors and few resiliency factors associated with violence. We found family violence in all 16 cases, including severe physical and/or sexual abuse in 14 cases; individual impairments in 16, including 14 with post-traumatic stress disorder, 13 with severe depression and 12 with histories of traumatic brain injury; community isolation and violence in 12; and institutional failure in 15, including 13 cases of severe physical and/or sexual abuse while in foster care or under state youth authority jurisdiction. Appropriate interventions might have made a difference in reducing lethal violence and its precursor conditions.

'In the safety of your own home': results from a national survey on gun use at home.

In the US, guns, particularly handguns, are typically brought into the home for protection. The wisdom of having a firearm in the home, however, is disputed. While guns appear to be a risk factor for family homicide, suicide and unintentional firearm fatality, no evidence has been available about gun use at home to intimidate family members and little about gun use to thwart crimes by intruders, or about the use of other weapons in home self-defense. Over the past decade, various private surveys have asked questions about the respondent's use of guns in self-defense. None, however, has asked detailed questions about the use of guns to threaten or intimidate the respondent. This study presents results from a national random digit dial telephone survey of 1906 US adults conducted in the spring of 1996. Respondents were asked about hostile gun displays and use of guns and other weapons in self-defense at home in the past five years. The objective of the survey was to assess the relative frequency and characteristics of weapons-related events at home. Thirteen respondents reported that a gun was displayed against them at home, two reported using a gun in self-defense at home, and 24 reported using another weapon (e.g. knife, baseball bat) in home self-defense. While we do not always know whose weapon was used in these incidents, most gun brandishings were by male intimates against women. A gun in the home can be used against family members or intruders and can be used not only to kill and wound, but to intimidate and frighten. This small study provides some evidence that guns may be used at least as often by family members to frighten intimates as to thwart crime, and that other weapons are far more commonly used against intruders than are guns.

The public health approach to motor vehicles, tobacco, and alcohol, with applications to firearms policy.

The public health approach that has been used to reduce problems caused by motor vehicles, tobacco and alcohol is applied to firearms policy. Manufacturers try to focus prevention efforts on the user rather than the product, and promote education and law enforcement policies directed toward the consumer. Public health efforts emphasize the systematic collection of data, scientific inquiry, and a multi-faceted policy approach that includes modifying the product and the environment. The endeavor to reduce gun violence is part of the general and continuing public health struggle to reduce harms caused by consumer products.

Inhalation of acid coated carbon black particles impairs alveolar macrophage phagocytosis.

A flow-past nose-only inhalation system was used for the co-exposure of mice to carbon black aerosols (CBA) and sulfur dioxide (SO2) at varying relative humidities (RH). The conversion of SO2 to sulfate (SO4(-2)) on the CBA, at a fixed aerosol concentration, was dependent on RH and SO2 concentration. The effect of the aerosol-gas mixture on alveolar macrophage (AM) phagocytosis was assessed three days following exposure for 4 h. Exposure to 10 mg/m3 CBA alone at low RH (10%) and high RH (85%), to 10 ppm SO2 alone at both RH, and to the mixture at low RH had no effect on AM phagocytosis. In contrast, AM phagocytosis was significantly suppressed following co-exposure at 85% RH, the only circumstance in which significant chemisorption of the gas by the aerosol and oxidation to SO4(-2) occurred. The results suggest that fine carbon particles can be an effective vector for the delivery of toxic amounts of SO4(-2) to the periphery of the lung.

Silicosis in mice: effects of dose, time, and genetic strain.

Experimental silicosis allows study of the mechanisms of lung injury, inflammation, and fibrosis. Inbred mice are an attractive species in which to study these mechanisms because of recent progress in murine immunology, molecular biology, and genetics. We exposed mice to an aerosol of silica and examined the effects of exposure dose, the evolution of disease features over time, and the variation in responses among four inbred strains. In C3H/HeN mice incremental cumulative exposure doses of cristobalite silica caused increased initial lung dust burden 12 to 16 weeks post-exposure, progressively intense pathological responses, and increased total lung collagen (hydroxyproline). The histopathological changes and total lung collagen increased progressively over time after exposure. We compared the features of silicosis in four strains of inbred mice selected for common use or immunologic reactivity 16 weeks after aerosol inhalation exposure to crystalline cristobalite silica (70 mg/m3, 5 hours/day, 12 days). C3H/HeN mice demonstrated histopathological silicotic lesions and enlarged intrapulmonary lymphoid tissue, and increased lung wet weight, bronchoalveolar lavage (BAL) recovery of macrophages, lymphocytes, and neutrophils, and total lung collagen (hydroxyproline). BALB/c mice developed slight pulmonary lesions; MRL/MpJ mice demonstrated prominent pulmonary infiltrates with lymphocytes; New Zealand Black mice developed extensive alveolar proteinaceous deposits, inflammation, and fibrosis. Our findings demonstrate orderly dose-time-response relationships, and a substantial variation of responses among inbred strains of mice. This model should prove valuable for future experimental interventions into the mechanisms of silicosis.

Persistent overexpression of interleukin-1beta and tumor necrosis factor-alpha in murine silicosis.

The cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNFalpha), derived from macrophages and other cells, may promote mononuclear cell inflammation and fibrosis in pulmonary silicosis. C3H/HeN mice were exposed to control air or to an aerosol of 70 mg/m3 cristobalite silica for 5 h/d for 12 days and examined at 2 and 16 weeks after exposure. This exposure resulted in murine silicosis, as manifested by focal mononuclear cell accumulations, diffuse interstitial fibrosis, lymphoid tissue enlargement, recruitment of inflammatory cells into BAL fluid, and increased total lung collagen. Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) with designed primers and membrane hybridization with biotinylated cDNA probes were used to assess the abundance of IL-1beta and TNFalpha mRNA. In situ hybridization with digoxigenin-labeled cDNA probes was used to localize gene expression. Persistent overexpression of both IL-1beta and TNFalpha were found at 2 and 16 weeks in the lungs of silica-exposed mice compared with air-sham control mice. IL-1beta and TNFalpha expression localized to individual mononuclear cells in the alveolar spaces, groups of cells within the aggregate lesions, and scattered mononuclear cells in BALT and lymphoid nodules. Thus, cells producing IL-1beta and TNFalpha appear to be intimately associated with the evolving lesions of silicosis, and the lymphoid tissue of the lung may be important in driving the pathogenesis of this disease.

Lymphocytes, lymphokines, and silicosis.

Silicosis is characterized by mononuclear cell aggregation with mineral particles and fibrosis. Lymphocytes are abundant in these lesions. We exposed inbred strains of mice to a respirable aerosol of cristobalite silica (70 mg/m3, 5 h/d, 12 d) or shamair. Silicosis evolved over months after exposure. The silica-exposed mice showed the accumulation of lymphocytes in alveolar spaces (seen in bronchoalveolar lavage), in lung parenchymal lesions and nodules, and in enlarged bronchial-associated lymphoid tissues and thoracic lymph nodes. The lung lymphocytes were predominantly CD4+ T cells, but numerous CD8+ T cells, natural killer cells, and CD4- gammadelta-TCR+ T cells were present as well. Interferon-gamma (IFN-gamma) production was upregulated, suggesting a THelper-1-like response in silicosis. In silicotic lung tissue, mRNA transcripts for the macrophage-derived cytokines IL-12 and -18 were increased. IFN-gamma gene-deleted mice (C57Bl/6-Ifngtm1 Ts) exposed to silica developed less extensive silicosis and less lung collagen accumulation than wild-type mice. We hypothesize that there is a reiterative amplification cycle in which macrophages with silica may produce cytokines, such as IL-12 and -18, that attract and activate lymphocytes. These activated lymphocytes may then produce additional mediators that in turn attract and activate an expanded secondary population of macrophages. IFN-gamma would be a likely cause of macrophage activation in this cycle. More work is needed to understand the biological events that lead from the inhaled dust to the scarred lung, and to clarify the role of lymphocytes in this process.

Fuzzy dice, dream cars, and indecent gestures: correlates of driver behavior?

In 1989 the Los Angeles Times conducted a telephone survey of over 1,800 Southern California motorists. We analyzed the data to determine whether personality and demographic characteristics were related to driver behavior. Fourteen percent of drivers were involved in a motor vehicle accident in the previous year, 8% reported driving when they had too much to drink, 20% ran at least one red light in the previous month, and nearly half said they often drove faster than the speed limit. Motorists under 30 years of age are especially likely both to engage in the three risk-taking behaviors and to be involved in a crash, even holding other factors constant. Drivers over 65 years of age take fewer risks, but have the same likelihood of having an accident per mile driven as middle-aged motorists. Surprisingly, drivers with more than a high school education are more likely to both speed and be involved in a crash. Those with fuzzy dice or bumper stickers are not readily distinguishable from other motorists in terms of accidents or risk-taking behaviors. Individuals driving their dream car are somewhat less likely than others to run red lights and drive after drinking. Motorists who made indecent gestures at other drivers, and particularly those who argue with other motorists tend to be unlawful and dangerous drivers. Youth and hostility toward other motorists are two of the most significant and important correlates of bad driving.