[Driving under the influence of medication and various substances other than alcohol].
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The dangers of medication for traffic safety have been vastly underestimated in modern society. The widespread and ever-growing use of medical drugs - in particular psychopharmaca - without a thought given to how these drugs may affect the ability to drive a car, gives a clear indication that it is time to take a close look at the problem. This article focuses on the civil liability under German law for traffic accidents resulting from the use of medication. Basically, three potential defendants come to mind when one searches for addresses of claims for damages. Apart from the driver himself or herself, these are the doctor who prescribed the drug and the manufacturer who manufactured the drug. This article argues that - at least from a German law perspective - in many cases it will ultimately make more sense to include the doctor (on a negligence liability theory) and the drug manufacturer (on a strict liability theory) as defendants in an action for damages than merely to go after the obvious perpetrator, namely the driver.
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Legally, alcohol and "other intoxicating substances" are given the same treatment (sections 315 c para. 1 letter a, 316 StGB). This implies that the findings of the German Public Health Office with regard to alcohol on the road should serve as methodical guidelines for medical findings when judging driver fitness after drug use. Therefore limits for "absolute" driver incapability after drug use can only decided on after special consideration of the outcome of attempts to drive. In addition, the basis of simultaneous results of the same rank of the biological-medical as well as the statistical research of the different psychotropic substances have to be taken into consideration. There is still a lack of proven results about the relation between dose, blood concentration and effect, which enabled the determination of limits. Therefore the emphasis of the medico-toxicological examination lies in the interpretation of the psycho-physical state of the driver at the time of being stopped and of the blood examination, as well as the blood-active substances-concentration with regard to the "relative" driver incapability.
A driver was found asleep behind the steering wheel of his car, and the vehicle was at rest in a traffic lane with the engine running. His manifestations included horizontal and vertical gaze nystagmus, muscle flaccidity, and severe ataxia. He admitted ingesting a white powder, which he identified as an amino acid, about 1 hour prior to discovery by police. A urine specimen collected approximately 1 hour after the traffic stop contained 1975 mg/L of gamma-hydroxybutyrate (GHB). We tentatively conclude that GHB may cause impairment of the psychomotor skills required for safe operation of a motor vehicle.
This study uses Golgi-impregnated material to examine the effects of altering the nature of afferent driving on the maturation of spines and dendrites on thalamic recipient spiny stellate neurons in layers 4C alpha and beta of the monkey striate cortex. These two laminae receive input from different sets of thalamic afferents with different functional properties. The development of dendritic spine and dendritic branch populations on these neurons in experimental animals is compared to the same features on similar groups of neurons in a series of normal animals described in the preceding study (Lund and Holbach, '91). Three conditions of rearing were used to alter afferent driving from normal: complete darkness (with in some cases return to normal diurnal light-dark cycle), bilateral eye lid suture, and monocular eye lid suture. Some of the normal and dark-reared infant monkeys were examined behaviorally for visual capacity in an earlier study (Regal et al., '76). All conditions of abnormal afferent driving caused changes from the normal developmental patterns of spine and dendritic arbor growth in these first-order neurons of the cortex and each condition differed in the nature of change produced. Major findings of this study are: 1. Vigorous spine acquisition and dendritic growth occurs under all conditions of visual deprivation on alpha and beta neurons. Eventual spine and dendritic attrition occurs under at least conditions of bilateral or monocular lid suture to produce a rather constant adult morphology. We assume, therefore, that visually driven activity is a modulator or shaper of the developmental process for thalamic recipient neurons of visual cortex, rather than being an initiator, terminator, or driving force for their maturation. 2. An innate "clock," whose nature is unknown but is apparently not driven by visual input, initiates and terminates a period of growth of the thalamic recipient neurons between birth and 30-32 weeks of age. 3. Factors controlling dendritic arbor growth and retraction are different from those controlling spine synapse addition or attrition. 4. Whereas the alpha and beta neurons normally show quite different early growth patterns between birth and 30 weeks of age, when both eyes are simultaneously deprived of vision, an early temporal and numerical convergence occurs in patterns of spine population development on the two groups of neurons. This convergent pattern assumes a different form in dark-reared and lid-sutured animals.(ABSTRACT TRUNCATED AT 400 WORDS)
Nitrogen oxides (NOx) and polycyclic aromatic hydrocarbons are common air pollutants generated from automobile exhaust and cigarette smoke. This study was to investigate urinary 8-hydroxydeoxyguanosine (8-OHdG) as an effective biomarker on DNA damage from traffic exhaust and/or smoking in exposed and non-exposed individuals. With subject consents, the levels of plasma NOx, urinary 1-hydroxypyrene (1-OHP) and 8-OHdG were determined for 95 male taxi drivers and 75 male community residents as the reference group. After adjusting for associate variables, there was a significant correlation between the levels of urinary 8-OHdG and 1-OHP but not NOx. The average level of urinary 8-OHdG was significantly higher in drivers than in community men (13.4+/-4.7 vs. 11.5+/-4.7 microg/g creatinine in mean+/-standard deviation). Compared with non-smoking community men, the multivariate logistic regression showed that the odds ratios (OR) of having elevated levels of urinary 8-OHdG (greater than the overall median value, 12.1 microg/g creatinine) were 6.6 (95% confidence interval (CI)=2.1-20.8) for smoking community men, 5.0 (95% CI=1.7-14.7) for non-smoking taxi drivers and 4.6 (95% CI=1.4-15.0) for smoking taxi drivers. Higher risk was also observed for areca quid chewers compared with non-chewers (OR=1.6; 95% CI=1.1-3.6). In conclusion, taxi driving and smoking may contribute independently to elevated DNA damage using urinary 8-OHdG levels as a sensitive biomarker. This effect is most potent on heavy smokers.
To determine whether the responses of tracheal smooth muscle and the nasal vasculature to stimulation of lung C-fiber receptors depend on the level of respiratory drive, the effects of right atrial injection of capsaicin and phenyldiguanide were studied in chloralose-anesthetized, paralyzed, artificially ventilated cats. Studies were performed while the animals were hyperventilated to apnea and, in addition, when breathing was stimulated by inhalation of 7% CO2 or by N-methyl-D-aspartic acid (NMDA) applied to the ventral surface of the medulla. When the cats were hyperventilated to apnea with O2, injection of capsaicin into the right atrium increased tracheal tone and slightly raised nasal resistance. However, when the animals were ventilated with 7% CO2 in O2 or respiratory activity was stimulated by the application of NMDA, administration of capsaicin eliminated spontaneous phrenic nerve activity and caused an abrupt decrease in tracheal tone but still increased nasal resistance. Similar responses were also obtained with right atrial injection of phenyldiguanide. These results showed for the first time that in the cat the direction of the reflex effects on tracheal tone but not nasal resistance depends on the preexisting level of respiratory drive and on cholinergic activity to airway smooth muscle.
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On a regular basis, the media presents the potential risks of the use of psycho-active compounds, including misused pharmaceuticals (flunitrazepam, GHB) or drugs of abuse (cannabis, LSD, ecstasy). Ethanol is also frequently encountered. These drugs can be used for recreational purposes by addicts or can be observed after sexual assaults (drugs spiked in food). Forensic toxicology can be involved in several situations to document impairment, such as: crime under influence, date rape, driving under influence, psychiatric disorders, determination of the cause of death... In some particular situations, it can be very cautious to investigate exposure to psycho-active drugs, due to late sampling of biological specimens. To enhance the window of detection of 3 specific drugs, the authors propose the following: 1. Use of an ultra-sensitive technique, such as GC/MS/MS/NCI for 7-aminoflunitrazepam; 2. Use of a cumulative specimen, such as sweat for GHB and 3. Use of a metabolite with a long half-life, such as ethyl glucuronide for ethanol.
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