Using safety data to describe common injury-producing events examples from the U.S. Air force.

BACKGROUND: The U.S. military leadership has recently increased its efforts to reduce the number of lost-workday injuries for both the active duty and civilian employee components of the total force. The detailed causes and circumstances of those nonfatal injuries-information needed for injury prevention-has largely been unexplored. The purpose of this project was to determine the utility of Air Force safety data for nonfatal injury prevention. METHODS: In 2004, events associated with injury-producing mishaps reported through the U.S. Air Force (USAF) Ground Safety Automated System from 1993-2002 (n = 32,812 injuries) were reconstructed. Essential data elements necessary to reconstruct event causes and circumstances were identified in both coded data and in free-text mishap narratives. Activities and mechanisms were coded in a format similar to that of the ICD-10. A taxonomy was then developed to identify hazard scenarios associated with injury-producing activities or mechanisms. RESULTS: Coded data provided only four data elements (activity, injury event/exposure, nature of injury/body part, and outcome) that were sufficiently descriptive for prevention purposes. Therefore, narrative information was coded and analyzed to obtain additional information. The assembled data enabled identification and description of hazard scenarios associated with the most common injury-producing activities and mechanisms. CONCLUSIONS: Safety reports from the USAF provide detailed mishap descriptions for lost-workday injuries that could support in-depth analysis and more effective preventive efforts. However, some of the most valuable information is found in the pre-text narratives that require coding and classification, such as was conducted for this report in order to be optimally useful for injury epidemiology and prevention.

Mechanisms of slow-pitch softball injuries reported to the HQ Air Force Safety Center a 10-year descriptive study, 1993-2002.

BACKGROUND: Softball is a popular sport in civilian and military populations and results in a large number of lost-workday injuries. The purpose of this study is to describe the mechanisms associated with softball injuries occurring among active duty U.S. Air Force (USAF) personnel to better identify potentially effective countermeasures. METHODS: Data derived from safety reports were obtained from the USAF Ground Safety Automated System in 2003. Softball injuries for the years 1993-2002 that resulted in at least one lost workday were included in the study. Narrative data were systematically reviewed and coded in order to categorize and summarize mechanisms associated with these injuries. RESULTS: This report documents a total of 1181 softball-related mishap reports, involving 1171 active duty USAF members who sustained one lost-workday injury while playing softball. Eight independent mechanisms were identified. Three specific scenarios (sliding, being hit by a ball, and colliding with a player) accounted for 60% of reported softball injuries. CONCLUSIONS: Mechanisms of injury for activities such as playing softball, necessary for prevention planning, can be identified using the detailed information found in safety reports. This information should also be used to develop better sports injury coding systems. Within the USAF and U.S. softball community, interventions to reduce injuries related to the most common mechanisms (sliding, being hit by a ball, and colliding with a player) should be developed, implemented, and evaluated.

Mechanisms of basketball injuries reported to the HQ Air Force Safety Center a 10-year descriptive study, 1993-2002.

BACKGROUND: Basketball is the most popular sport among the U.S. Air Force (USAF) active duty population and causes a large number of lost-workday injuries. The purpose of this study is to describe how basketball injuries occur to allow development of effective countermeasures. METHODS: This study used data derived from safety reports obtained from the USAF Ground Safety Automated System. Basketball injuries for the years 1993-2002 that resulted in at least one lost workday were included in the study conducted in 2003. Narrative data from 32,818 safety reports were systematically reviewed and coded in order to categorize and summarize mechanisms associated with these injuries. RESULTS: A total of 2204 mishap reports involving active duty USAF members playing basketball were documented by the study. This study identified seven mechanisms causing basketball injury. Two similar causes involving jumping (landing awkwardly and landing on someone's foot) accounted for 43% of basketball injuries followed by collisions with other players (10%). CONCLUSIONS: This study shows that mechanisms of basketball-related injury can be identified using the detailed information found in USAF safety reports. Knowledge of leading hazards or mechanisms for basketball injuries can be used to prioritize and develop prevention strategies.

Mechanisms of flag-football injuries reported to the HQ Air Force Safety Center a 10-year descriptive study, 1993-2002.

BACKGROUND: Flag (touch or intramural) football is a popular sport among the U.S. Air Force (USAF) active duty population and causes a substantial number of lost-workday injuries. The purpose of this study is to describe the mechanisms of flag-football injuries to better identify effective countermeasures. METHODS: The data were derived from safety reports obtained from the USAF Ground Safety Automated System. Flag-football injuries for the years 1993-2002 that resulted in at least one lost workday were included in the study conducted in 2003. Narrative data were systematically reviewed for 32,812 USAF mishap reports; these were then coded in order to categorize and summarize mechanisms associated with flag football and other sports and occupational injuries. RESULTS: Nine hundred and forty-four mishap reports involving active duty USAF members playing flag football met the criteria for inclusion into this study. Eight mechanisms of injury were identified. The eight mechanisms accounted for 90% of all flag-football injuries. One scenario (contact with another player) accounted for 42% of all flag-football injuries. CONCLUSIONS: The most common mechanisms of injury caused by playing flag football can be identified using the detailed information found in safety reports. These scenarios are essential to developing evidence-based countermeasures. Results for flag football suggest that interventions that prevent player contact injuries deserve further research and evaluation. The broader implications of this study are that military safety data can be used to identify potentially modifiable mechanisms of injury for specific activities such as flag football.

Injuries to air force personnel associated with lifting, handling, and carrying objects.

BACKGROUND: The U.S. Air Force (USAF) active duty and civilian populations experience a substantial number of lost-workday injuries while lifting, handling, and carrying objects. Back injuries are most frequently reported. PURPOSE: The purpose of this study is to describe the hazard scenarios of lift-handle-carry injuries to better identify effective countermeasures. METHODS: The data were derived from safety reports obtained from the USAF Ground Safety Automated System. Lift-handle-carry injuries for the years 1993-2002 that resulted in at least one lost workday were included in the study. A total of 4085 lost-workday injuries resulting in 24,940 lost workdays for USAF military and civilian members met the criteria for inclusion. Objects associated with these injuries were identified and aggregated to determine the most common causes of lift-handle-carry injuries. RESULTS: Twelve distinct objects or type of objects were identified as the most common source of lift-handle-carry injuries. Among the most common sources of injury were lifting aircraft components, boxes, and furniture. Most importantly, lifting one group of objects, aircraft components, was associated with 33% of all lift-handle-carry injuries. CONCLUSIONS: Safety report data can be used to identify the most common object or object types causing lift-handle-carry injuries. The information included in this report suggests countermeasures that should be considered for implementation and evaluation studies. Countermeasures to address the most common lift-handle-carry injuries, such as lifting aircraft components among aircraft maintenance workers, are warranted.

Mesenteric vasoconstriction and hindquarters vasodilatation accompany the pressor actions of exendin-4 in conscious rats.

The hemodynamic effects of the glucagon-like peptide-1 (GLP-1) receptor agonist, exendin-4, and putative underlying mechanisms were assessed in conscious male Sprague-Dawley rats. At a dose of 25 ng kg(-1) i.v., exendin-4 had little effect, but doses of 250 and 2500 ng kg(-1) had significant tachycardic effects (+66 +/- 9 and +95 +/- 16 beats min(-1) at 5 min, respectively) and pressor actions (+10 +/- 2 and +12 +/- 1 mm Hg), accompanied by substantial falls in mesenteric vascular conductance (-38 +/- 3% and -47 +/- 3%) and increases in hindquarters vascular conductance (+82 +/- 14% and +126 +/- 15%). The latter were likely due to adrenaline-mediated activation of beta(2) adrenoceptors since they were abolished by the beta(2) adrenoceptor antagonist, ICI 118551 [(+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol) hydrochloride], or propranolol [(RS)-1-[(1-methylethyl)amino]-3-(1-naphthalenyloxy)-2-propanol], and absent in adrenal-demedullated rats. In the presence of beta-adrenoceptor antagonism, the tachycardic effects of exendin-4 were suppressed, but the pressor action was enhanced. Enhancement of the pressor action of exendin-4 was not seen in adrenal-demedullated rats or in animals given phentolamine in addition to propranolol, consistent with a component of the pressor action of exendin-4 being due to an adrenaline-mediated positive inotropic effect mediated by alpha-adrenoceptors. The mesenteric vasoconstrictor effect of exendin-4 was unaffected by antagonism of alpha-adrenoceptors, vasopressin receptors, angiotensin receptors, or GLP-1 receptors, although antagonism of the latter substantially inhibited the hindquarter vasodilator effects of exendin-4. These results are consistent with exendin-4 having cardiovascular effects through GLP-1 receptor-dependent and -independent mechanisms, some of which involve sympathoadrenal activation.

Regional heterogeneity in the haemodynamic responses to urotensin II infusion in relation to UT receptor localisation.

The aim of the study was to measure regional haemodynamic responses to 6 h infusions of human urotensin II (hUII), to identify possible mediators of the effects observed, and to relate the findings to the distribution of urotensin II receptors (UT receptors). Male, Sprague-Dawley rats had pulsed Doppler flow probes and intravascular catheters implanted for measurement of regional haemodynamics in the conscious, freely moving state. Infusions of saline (0.4 ml h(-1)) or hUII (30, 300 and 3,000 pmol kg(-1) h(-1)) were given i.v. for 6 h, and the effects of pretreatment with indomethacin (5 mg kg(-1) h(-1)), N(G)-nitro-L-arginine methyl ester (L-NAME, 3 mg kg(-1) h(-1)) or propranolol (1 mg kg(-1); 0.5 mg kg(-1) h(-1)) on responses to hUII (300 pmol kg(-1) h(-1) for 6 h) were assessed. Cellular localisation of UT receptor-like immunoreactivity was determined in relevant tissues. hUII caused dose-dependent tachycardia and hindquarters vasodilatation, accompanied by a slowly developing rise in blood pressure. Haemodynamic effects of hUII were attenuated by propranolol or L-NAME and abolished by indomethacin. UT receptor-like immunoreactivity was detected in skeletal and vascular smooth muscle. The findings indicate that in conscious rats, infusions of hUII cause vasodilatation, which, of the vascular beds monitored, is selective for the hindquarters and dependent on cyclooxygenase products and nitric oxide. The pressor effect of hUII under these conditions is likely to be due to an increase in cardiac output, possibly due to a positive inotropic effect. UT receptor-like immunoreactivity present in skeletal muscle is consistent with the haemodynamic pattern.

Inhibition of chloride secretion in human bronchial epithelial cells by cigarette smoke extract.

Chronic bronchitis, a disease mainly of cigarette smokers, shares many clinical features with cystic fibrosis, a disease of altered ion transport, suggesting that the negative effects of cigarette smoke on mucociliary clearance may be mediated through alterations in ion transport. We tested the hypothesis that cigarette smoke extract would inhibit chloride secretion in human bronchial epithelial cells. In agreement with studies in canine trachea, cigarette smoke extract inhibited net chloride secretion without affecting sodium transport. We performed microelectrode impalements and impedance analysis studies to investigate the physiological mechanisms of this inhibition. These data demonstrated that cigarette smoke extract caused an acute increase in membrane resistances in conjunction with apical membrane hyperpolarization, an effect consistent with inhibition of an apical membrane anion conductance. After this acute phase, both membrane resistances decreased while membrane potentials continued to hyperpolarize, indicating that cigarette smoke extract also inhibited the basolateral entry of chloride into the cell. Furthermore, cigarette smoke extract caused an increase in mucin secretion. Therefore, the ion transport phenotype of human bronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia in which there is sodium absorption out of proportion to chloride secretion in the setting of increased mucus secretion.

Regional hemodynamic actions of selective corticotropin-releasing factor type 2 receptor ligands in conscious rats.

In conscious male Sprague-Dawley rats, we compared regional hemodynamic actions of the selective corticotropin-releasing factor type 2 (CRF(2)) receptor ligands human and mouse urocortin 2 (hUCN2 and mUCN2, respectively) with those of CRF. Bolus i.v. doses of 3 and 30 pmol kg(-1) hUCN2, mUCN2, or CRF had no significant hemodynamic actions, but at doses of 300 and 3000 pmol kg(-1), all three peptides caused dose-dependent tachycardia and hypotension, with rapid-onset, short-duration, mesenteric vasodilatation and slower-onset, more prolonged hindquarters vasodilatation but little or no change in renal vascular conductance. Pretreatment with the nonselective CRF receptor antagonist astressin or the selective CRF(2) receptor antagonist antisauvagine 30 abolished all the cardiovascular actions of all three peptides. Indomethacin had no effect on responses to hUCN2, and there was no evidence for any involvement of nitric oxide (NO) in the vasodilator actions of hUCN2. There was no evidence that recruitment of angiotensin- and endothelin-mediated vasoconstrictor mechanisms counteracted the vascular actions of hUCN2. The results indicate that the hemodynamic effects of i.v. hUCN2, mUCN2, and CRF depend on activation of CRF(2) receptors and do not involve NO or prostanoids.

Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response.

A biphasic cardiovascular response to bolus i.v. injection of human urotensin II (hUII, 3 nmol kg(-1)) in conscious, male, Sprague-Dawley (SD) rats was identified and underlying mechanisms were explored. Initially (0-5 min) there was tachycardia, hypotension and mesenteric and hindquarters vasodilatation; later (30-120 min), tachycardia, hindquarters vasodilatation and a modest rise in blood pressure occurred. Pretreatment with indomethacin or N(G) nitro-l-arginine methylester (l-NAME) reduced the mesenteric vasodilator response to hUII, and abolished the late tachycardia and hindquarters vasodilatation. Indomethacin also abolished the hypotension and early hindquarters vasodilatation, and substantially reduced the initial tachycardia. Indomethacin and l-NAME together prevented all haemodynamic responses to hUII. Inhibition of inducible NOS had no effect on responses to hUII, whereas inhibition of neuronal NOS reduced the delayed tachycardic response to hUII but did not significantly affect the vasodilatation. Only the initial tachycardic response to hUII was antagonised by propranolol. In spontaneously hypertensive rats (SHR), the initial haemodynamic responses to hUII were qualitatively similar to those in SD rats, although there was also a modest renal vasodilatation. The secondary response comprised a smaller tachycardia and a small rise in blood pressure, with no significant hindquarters vasodilatation. Haemodynamic responses to hUII were not enhanced by endothelin and angiotensin receptor antagonism in either SD rats or in SHRs. One interpretation of these results is that the primary response to bolus injection of hUII is prostanoid- or prostanoid- and NO-mediated (mesenteric vasodilatation) and that this triggers secondary events, which are dependent on eNOS (hindquarters vasodilatation) and neuronal NOS (tachycardia).

Nucleotide-mediated mucin secretion from differentiated human bronchial epithelial cells.

Most current cell-based models for examining the regulation of mucin secretion demonstrate low signal-to-noise ratios, making experimental manipulation and data interpretation difficult. Using adenosine triphosphate (ATP) as a mucin secretagogue, we have developed a model of agonist-induced mucin secretion in differentiated human bronchial epithelial cells. Mucin secretory signals were estimated using enzyme-linked lectin assay, and typical signals of 300-400% of baseline were observed in response to a 30-min exposure to ATP (100 microM). ATP and uridine triphosphate equipotently stimulated mucin secretion consistent with mediation via P2Y2 receptor activation. Suramin and AR-C118925XX, a competitive P2Y2 receptor antagonist, inhibited adenosine 5'-o-(3-thiotriphosphate) (ATP-gammaS)-induced mucin secretion. A selective Gq G-protein antagonist (GP-ANT)-2A completely abrogated ATP-gammaS-induced mucin secretion. Pertussis toxin and the G(i/o)-specific, GP-ANT-2, had no effect. The phospholipase C inhibitor, D609, and the protein kinase C inhibitor, calphostin C, substantially inhibited ATP-gammaS-induced mucin secretion. Phorbol myristate acetate also stimulated mucin secretion in a calphostin C-sensitive manner. ATP-gammaS-induced mucin secretion was inhibited by the Ca2+ chelator, 1,2-bis(o-aminophenoxy) ethane-N,N,N',N'-tetra-acetic acid tetra (acetoxymethyl) ester. Ionomycin and thapsigargin both stimulated mucin secretion. Our data are broadly consistent with known G-protein-coupling and downstream signaling events associated with the P2Y2 receptor. The exceptional signal-to-noise ratios obtained using this model have permitted clear evaluation of the involvement of these mechanisms in agonist-induced mucin secretion from differentiated human bronchial epithelial cells.

Haemodynamic effects of the selective phosphodiesterase 5 inhibitor, UK-357,903, in conscious SHR.

1. Regional haemodynamic responses to a continuous, 4-day infusion of the selective phosphodiesterase type 5 inhibitor, UK-357,903 (0.133 or 1.33 mg x kg(-1) h(-1)) were measured in conscious spontaneously hypertensive rats, and compared with those of enalapril (1 mg x kg(-1) h(-1)). 2. Both doses of UK-357,903 caused modest reductions in mean blood pressure that were not dose-dependent and only significantly different from the vehicle effects on Day 1 of the study (mean -11.8 and -15.3 mmHg for low and high doses, respectively). UK-357,903 had mesenteric and hindquarters vasodilator effects, which were, again, similar for both dose levels and only significantly different from vehicle on Day 1. Neither dose of UK-357,903 affected renal vascular conductance or heart rate. 3. Although the haemodynamic effects of UK-357,903 were not clearly dose-related and some appeared to wane with time, geometric mean plasma levels of UK-357,903 increased in proportion to dose, and were sustained throughout the infusion period. Furthermore, plasma cyclic guanosine monophosphate, a biomarker of phosphodiesterase 5 inhibition, was persistently elevated, and increased with increasing dose. 4. Enalapril caused a fall in mean blood pressure on day 1 (-14.1 mmHg) that was associated with dilatation in renal, mesenteric and hindquarters vascular beds. The haemodynamic effects of enalapril were sustained or increased over the 4-day infusion, although plasma free drug levels were stable. 5. In conclusion, we have shown regional and temporal changes in the haemodynamic effects of UK-357,903, which may be due to activation of compensatory mechanisms, but there were no signs of functional compensation to the cardiovascular effects of enalapril.

Comparative regional haemodynamic effects of the nitric oxide synthase inhibitors, S-methyl-L-thiocitrulline and L-NAME, in conscious rats.

1. The regional haemodynamic effects of the putative nNOS inhibitor, S-methyl-L-thiocitrulline (SMTC), were compared with those of the nonselective NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), in conscious, male Sprague-Dawley rats. 2. SMTC (0.3 mg kg(-1) bolus) produced a significant, short-lived, pressor effect associated with renal, mesenteric and hindquarters vasoconstriction; the same dose of L-NAME did not affect mean blood pressure (BP), although it caused bradycardia and mesenteric vasoconstriction. 3. At the highest dose tested (10 mg kg(-1)), L-NAME produced a significantly greater bradycardia and fall in mesenteric vascular conductance than SMTC, although the initial pressor response to SMTC was greater, but less sustained, than that to L-NAME. 4. Infusion of SMTC or L-NAME (3 mg kg(-1) h(-1)) induced rises in BP and falls in renal, mesenteric and hindquarters vascular conductances, but the effects of L-NAME were greater than those of SMTC, and L-NAME also caused bradycardia. 5. The renal vasodilator response to acetylcholine was markedly attenuated by infusion of L-NAME, but unaffected by SMTC. The hindquarters vasodilatation induced by salbutamol was attenuated by L-NAME, but not by SMTC. The mesenteric vasodilator response to bradykinin was modestly enhanced by SMTC, but not by L-NAME. The depressor and renal, mesenteric and hindquarters vasodilator responses to sodium nitroprusside were enhanced by L-NAME, whereas SMTC modestly enhanced the hypotensive and renal vasodilator effects of sodium nitroprusside, but attenuated the accompanying tachycardia. 6. The results are consistent with the cardiovascular effects of low doses of SMTC being attributable to nNOS inhibition.