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Interactive Effects of Ammonia and Light Intensity on Hematochemical Variables in Broiler Chickens¹

H. A. Olanrewaju^*,2, J. P. Thaxton, W. A. Dozier, III^*, J. Purswell^*, S. D. Collier^* and S. L. Branton^*

^* USDA, Agricultural Research Service, Poultry Research Unit, PO Box 5367, Mississippi State, MS 39762-5367; and Department of Poultry Science, Mississippi State University, Mississippi State 39762-9665

² Corresponding author: Hammed.Olanrewaju{at}ars.usda.gov

	ABSTRACT

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This study examined the influence of early atmospheric ammonia exposure, light intensity throughout rearing, and their interaction on blood gases, electrolytes, and acid-base balance in broiler chickens under environmentally controlled conditions. The experiment consisted of a 3 x 3 factorial arranged in a randomized complete block design, with trials being replicated over time. The 9 treatments consisted of 3 levels (0, 25, and 50 ppm) of ammonia concentrations for 14 d and levels (0.2, 2.0, and 20 lx) of light intensities from 8 to 36 d of age. Venous blood samples were collected on d 6, 11, 14, and 35. On d 6, partial pressure of CO₂ and Na⁺ increased significantly (P 0.05), whereas partial pressure of O₂, pH, and K⁺ decreased with increasing ammonia concentration. As light intensity increased, pO₂ and K⁺ were significantly (P 0.05) reduced. Ammonia x light intensity interactions were observed for hemoglobin, hematocrit, K⁺, and BW. The interaction of ammonia and light intensity for 7 d further exacerbated physiological variables. The main effect of ammonia was more pronounced than that of light intensity. These conditions worsened as the duration of ammonia concentration exposure and light intensity increased from d 7 to 14 of exposure. However, all affected variables returned to near normal at later time points in the exposed chickens so that the apparent effects were lost. Plasma corticosterone and glucose concentrations were not significantly altered by exposure to differing levels of ammonia or light intensity, suggesting an absence of stress related to ammonia, light intensity, or their interaction. It was concluded that exposure of broiler chickens to aerial ammonia concentrations of 0 to 50 ppm from d 1 to 14 posthatch in the presence of light intensities ranging from 0.2 to 20 lx had no direct effect on some physiological blood variables and did not induce stress in broilers.

Key Words: ammonia • light intensity • acid-base balance • broiler • well-being

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCE

 
Atmospheric ammonia (NH₃) has been shown to be detrimental to poultry health and performance (Carlile, 1984; Kristensen and Wathes, 2000) and is cited as an environmental concern as well (NRC, 2003; USDA, 2005). Exposure to high concentrations of NH₃ (>50 ppm) causes keratoconjunctivitis, with symptoms including watery eyes, closed eyelids, rubbing of eyes with the wings, and blindness (Bullis et al., 1950; Faddoul and Ringrose, 1950). Our recent study indicated that eye damage induced by the interaction of NH₃ and light intensity decreased significantly beginning 1 wk after cessation of NH₃ exposure (Olanrewaju et al., 2007a). In addition, from the same study, fear and leg health was not affected by NH₃, light intensity, or their interaction. However, effects on physiological variables of exposure of broilers to high NH₃ concentrations is not well understood. The effects of NH₃ toxicity on blood pH have been variously described as respiratory acidosis or metabolic alkalosis in cattle (Rash et al., 1968; Davidovich et al., 1977) and as metabolic acidosis in sheep (Lyoyd, 1970).

Lighting programs that decrease the photoperiod have been shown to minimize skeletal disorders and metabolic diseases, such as sudden death syndrome and ascites (Classen et al., 1991; Renden et al., 1991). Low light intensities have also shown benefits in broiler growth (Charles et al., 1992). However, welfare consultants have expressed concerns that low light intensity (0.2 lx) may cause damage to the eye lens or lead to blindness (Ashton et al., 1973; Chiu et al., 1975; Cummings et al., 1986; Buyse et al., 1996). Both light intensity and NH₃ exposure, which have been associated with blindness, influence the functional development of the eye. Although we now have a good understanding of how lighting, particularly photo-period, affects poultry production, our knowledge of the effect of light intensity on the visual abilities of broilers and the involvement of blood gases, electrolytes, and acid-base balance on the welfare of birds are shallow by comparison.

Removing or reducing all sources of stress fundamentally affects how poultry utilize their energy. Elevated blood plasma corticosterone (CS) is widely used as a measurement of the environmental stress condition in birds (McFarlane and Curtis, 1989; Olanrewaju et al., 2006, 2007b). Physiological stress is associated with changes in acid-base status, and a range of functional and environmental stressors influence the acid-base balance of any animal. The objective of the present study was to evaluate the interactive effects of NH₃ and light intensity on blood gases, electrolytes, and acid-base balance, and their involvement in the welfare of broiler chickens. We hypothesized that inhalation of ambient air with elevated NH₃ concentrations under different light intensities may adversely affect the physiological blood variables and welfare of broiler chickens.

	MATERIALS AND METHODS

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Bird Husbandry

In each of 2 trials, 792 one-day-old Ross x Ross 708 (Aviagen Inc., Huntsville, AL) chicks were purchased from a commercial hatchery and randomly distributed into 9 environmentally controlled chambers (44 male and 44 female chicks/chamber). Each environmental chamber had a floor area of 65 ft² [7.6 x 8.5 ft (2.3 m x 2.6m) with a chamber volume of 541 ft³ [8.33-ft (2.5 m) ceiling]. Chicks were vaccinated for Marek’s, Newcastle, and infectious bronchitis diseases at the hatchery. Each chamber contained fresh pine shavings, tube feeders, and a 7-nipple watering system. Birds were provided a 3-phase feeding program (starter: 1 to 15 d; grower: 16 to 28 d; finisher: 29 to 36 d). Diets were formulated to meet or exceed NRC (1994) nutrient recommendations. Starter feed was provided as crumbles, and subsequent feeds were provided as whole pellets. Feed and water were offered ad libitum. Ambient temperature was maintained at 33°C at the start of experimentation and was reduced as the birds progressed in age, with a final temperature of 21°C at 35 d and thereafter. However, NH₃ concentrations in control (0 ppm) chambers from d 1 to 14 ranged from 0 to 4.7 ppm.

Treatments

The treatments consisted of exposure to 0, 25, or 50 ppm of NH₃ for 14 d from d 1 and exposure to 0.2-, 2.0-, or 20-lx light intensities from 8 to 36 d of age. The light intensity from d 0 to 7 was 20 lx in each chamber. Each chamber was equipped with incandescent lighting typical of that used in commercial housing. The light fittings and tubes were dusted weekly to minimize dust buildup that would otherwise reduce the intensity. Ammonia was metered into 6 of the 9 chambers at 25 or 50 ppm from 1 to 14 d of age, whereas the remaining 3 chambers served as controls (0 ppm). Each of the 3 NH₃-level treatments was paired with 1 of the 3 light-intensity treatments so that each chamber represented a particular NH₃ concentration: light-intensity level combination.

NH₃ Addition

For quantitative control of NH₃ concentration in the chambers, birds were placed on fresh pine shavings that were 10 cm deep at the beginning of each trial, and procedures for NH₃ administration were used that were similar to those in previous NH₃ studies conducted by Miles et al. (2004, 2006) at this laboratory. Anhydrous NH₃ was continuously metered into 6 of the chambers to maintain 3 chambers each at 25 and 50 ppm through panel-mount flow meters. No NH₃ (0 ppm) was added to the remaining 3 chambers that served as controls.

Ammonia was measured daily at 0800, 1200, 1600, and 2000 h during the first 4 d and once a day thereafter through d 14 with a photoacoustic multigas analyzer (Innova-1312, Air Tech Instruments, Ballerup, Denmark). Ammonia level was measured each day by animal caretakers before and again once or twice after disturbing the chamber atmosphere. During the 14-d exposure period, the average measured NH₃ concentration for each treatment level approximated the designated level, but variability with concentration increased because of the association of atmospheric NH₃ with that excreted in the shavings. The NH₃ levels ranged from 0 to 4.71 ppm for the control treatment (0 ppm), 24.73 to 25.43 ppm for the 25-ppm treatment, and 49.84 to 50.99 ppm for the 50-ppm treatment. The average concentrations for the 25- and 50-ppm treatments were 25.2 and 50.3 ppm, respectively.

BW, Blood Collection, and Chemical Analyses

Body weights were determined on d 1, 11, 14, 28, and 35. On d 6, 11, 14, and 35, blood samples were collected between 0800 and 0900 h on sampling day from a brachial vein of 5 randomly selected birds from each chamber, and the birds were then returned to the appropriate chambers by using our standard handling procedure (Olanrewaju et al., 2007a,b). In addition, unnecessary discomfort to the birds was avoided by using proper housing and handling techniques, as described by the NRC (1996). Blood samples were collected directly into heparinized (50 IU/mL) monovette syringes. All bleedings were completed within 45 s after birds were caught. Blood samples were drawn directly from the syringes into a blood gas-electrolyte analyzer (ABL-80 Flex, Radiometer America, Westlake, OH) for immediate analysis of partial pressure of CO₂ (pCO₂), partial pressure of O₂ (pO₂), pH, hematocrit (Hct), hemoglobin (Hb), and electrolytes (Na⁺, K⁺, Ca²⁺, HCO₃^–, and Cl^–). The pH, pCO₂, pO₂, and HCO₃^– values were corrected to reflect a body temperature of 41.5°C (Burnett and Noonan, 1974). The needle mounted on each monovette syringe was then removed, a cap was placed over the needle port, and the syringes containing the blood samples were plunged into ice.

After all birds were bled, the iced samples were transferred to the laboratory, centrifuged at 4,000 x g for 20 min, and the packed blood cells were expelled from the syringes. The plunger on each monovette was broken off and the syringe served as a storage vial for the remaining plasma. This procedure ensured that the plasma samples were never exposed to ambient air. Plasma samples were stored at –20°C for later chemical analysis. Plasma samples were removed from the freezer, thawed, and each sample was analyzed for corticosterone (CS) and glucose (GLU). Concentrations of plasma glucose were determined by using an autoanalyzer (Vitro DT 6011, Ortho-Clinical Diagnostic, Rochester, NY). This analyzer uses the enzymatic procedures described by Elliott (1984). Plasma CS was measured by using a universal microplate spectrophotometer (Bio-Tek Instruments Inc., Winooski, VT) with ELISA reagent assay test kits from Assay Designs (EIA-CS Kit, Assay Designs Inc., Ann Arbor, MI), according to the manufacturer’s instructions.

Statistical Analysis.

A 3 x 3 factorial arranged in a randomized complete design was used in this study. Data were replicated over time, with trial being the blocking factor. Chamber was considered the experimental unit. The 9 treatments consisted of 3 levels of NH₃ concentrations x 3 levels of light intensity. The main effects of NH₃ and light intensity and the interaction of these 2 factors on physiological variables were tested by using the MIXED procedure of SAS (SAS Institute, 2004). Means comparisons on d 6, 14, 28, and 35 were assessed by least significant differences, and statements of significance were based on P 0.05.

	RESULTS

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The influence of atmospheric NH₃ exposure, light intensity, and their interaction on plasma pH and HCO₃ is presented in Table 1. The NH₃ had a significant (P 0.05) effect on pH on d 6 and 35, especially for the 50-ppm level of NH₃ exposure. The main effect of light intensity on pH was not observed on any of the sampling days. Ammonia at 50 ppm reduced pH on d 6, whereas it increased pH on d 35. Furthermore, there was no significant effect of NH₃ exposure and light intensity on HCO₃ on any of the sampling days. There was also no interactive effect of NH₃ x light intensity on either pH or HCO₃ on any of the sampling days. The light intensity effect on pH and HCO₃ only approached significance on d 14, at P = 0.063, and on d 35, at P = 0.064, respectively. The main effect of NH₃ at 50 ppm caused a significant (P 0.05) increase in pCO₂ only on d 6, compared with 0 ppm, but was not different between 25 and 50 ppm (Table 2). Both NH₃ and light intensity significantly (P 0.05) reduced pO₂, especially on d 6 with 50 ppm of NH₃ exposure, whereas the main effect of light intensity at the 20-lx level on d 6 and 35 significantly reduced pO₂. There was no interactive effect of NH₃ x light intensity on either pCO₂ or pO₂ on any of the sampling days.

	DISCUSSION

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Results suggest an increased respiratory rate in broilers exposed to greater levels of NH₃, with or without light intensity. This may be attributed to mild metabolic acidosis, which has been associated with a minor reduction of pH and of HCO₃ concentration, along with sustained plasma Ca²⁺. However, decreased pO₂ may account for the metabolic acidosis because of anaerobic glycolysis or accumulations of carbonic and other intracellular acids. Acid-base disturbances may be a consequence of polypnea or panting, leading to hyperventilation and elimination of CO₂, which may result in hypocapnic alkalosis. However, NH₃ can combine with available water to form a base, thereby raising blood pH moderately (Roller, 1966; Roller et al., 1982). On the other hand, if NH₃ is released through the lungs, respiration produces an acute edema, carbonic acid accumulates to decrease blood pH, and a hypoxic condition develops. As was observed in this study, the increased pCO₂ may account for respiratory hyperpnea, which fails to prevent pO₂ from decreasing. The theoretical prediction is that metabolic alkalosis is significantly compensated for by an increase in plasma CO₂ resulting from a change in intrapulmonary chemoreceptors (Burger et al., 1974). The finding that the pH was elevated and plasma pCO₂ was changed slightly indicates minimal metabolic alkalosis. It is generally agreed that a decrease in plasma pH results in increased ventilation capacity and is partially responsible for metabolic acidosis compensation (Davenport, 1950). However, any speculation regarding the role of blood pH in the regulation of respiration must be tempered by a consideration of other factors that are also influential in the chemical control of respiration (Gesell, 1925). Increases in Hb and Hct, along with reduced blood oxygen saturation, as observed in this study, may be related to the increased metabolic activity needed to meet the energy demands for both maintenance and growth under relatively stressful conditions, leading to an increase in erythropoiesis as a compensatory reaction to the lack of oxygen in the tissues, possibly because of an impaired oxygen-carrying capacity in the blood or perhaps other yet unidentified factors.

Changes in the acid-base balance of the blood may mediate the negative subjective state that, for the animals in Gesell (1925), Davenport (1950), and Burger et al. (1974), was associated with ammoniated environments. The pH of the blood is maintained within a very narrow range because sudden changes can result in cellular damage via protein ionization (Eckert, 1988). The essential electrolytes for the maintenance of the acid-base balance are sodium (Na⁺), potassium (K⁺) and chlorine (Cl^–). However, K⁺ is more involved in many metabolic processes, including the acid-base balance (Borges et al., 2007). Acid-base homeostasis is traditionally seen as involving 2 organs, the lungs and the kidneys, as a result of increased absorption or excretion. In agreement with our findings, plasma K⁺ concentration has been reported to decrease by approximately 60% within 2 h after sampling in pigeon blood and, to a lesser extent, by 30% in 2 h in chickens (Shideman et al., 1981), but to increase by 30% within 4 h in macaws (Harr, 2002).

In the present study, the lack of increase in plasma glucose during the 14 d of NH₃ exposure in combination with light intensity suggests direct endocrine involvement with normal glucose production, rather than impaired utilization. Hyperglycemia is induced in birds by high levels of endogenous or exogenous glucocorticoids (Hazelwood, 1986). In this study, blood CS increased linearly along with NH₃ concentrations from d 6 of exposure, and it decreased significantly by d 35 so that the apparent concentration response was lost on d 35, which may suggest an absence of stress related to NH₃, light intensity, or their interaction. Gustin et al. (1994) reported similar results for pigs exposed to aerial NH₃ concentrations ranging from 0 to 100 ppm for 6 d; there was no direct effect on plasma cortisol concentrations, suggesting an absence of major stress related to NH₃.

The main effect of NH₃ on BW was observed on d 11 and 14, respectively. However, there was a compensatory gain in BW after NH₃ exposure was discontinued, in agreement with other studies (Reece et al., 1981; Miles et al., 2004). Moreover, it has been shown that 50- and 75-ppm levels of NH₃ exposure from d 1 to 28 reduced BW at 4 wk of age but that a rebound in BW occurred after NH₃ treatment was discontinued, as indicated at 7 wk of age (Reece et al., 1981; Miles et al., 2004). In addition, Quarles and Caveny (1979) reported that BW and feed efficiencies of birds exposed to 50 ppm of NH₃ did not differ significantly from those of the control group at 8 wk of age. In other reports, researchers did not observe a compensatory gain in BW in birds exposed to NH₃ (Quarles and Caveny, 1979). Between d 1 and 11 of the study, the average BW was not influenced by light intensity, unlike NH₃. However on d 14, birds under 2.0-lx light intensity showed significantly (P 0.005) higher BW compared with light intensities of 0.2 and 20 lx. The 2.0-lx intensity may have encouraged less bird distraction and less physical activity. Body weight differences attributable to light intensity may reflect greater activity levels in birds exposed to a bright light of 20 lx, whereby more energy is expended for activity and less is partitioned to growth. Conversely, birds reared under 0.2 lx showed a temporary growth delay at an early age, which may have been due to limited access to feed and may have manifested as compensatory gain during the subsequent period. However, by d 28, the main effects on BW of NH₃, light intensity, or their interaction had disappeared. In no previous reports has an interaction been observed between NH₃ and light intensity, as was the case here. In this study, BW were greater and were similar in the 0-ppm NH₃ treatment along with different levels of intensity, whereas with the 50-ppm NH₃ treatment, BW were greater in combination with 2.0- and 20-lx light intensity, respectively.

We conclude that alterations of some blood physiological variables caused by NH₃ exposure rapidly cleared on cessation of NH₃ exposure while light intensity treatments were still ongoing. Further, NH₃ concentrations and light intensity apparently did not interact or acted independently to affect plasma CS, suggesting that these factors may not pose as stressors to the birds, although there is evidence in the literature that NH₃ or different lighting programs may influence physiological stress responses.

	ACKNOWLEDGMENTS

 
The authors thank M. Carden and L. Halford for their contribution to this research.

	FOOTNOTES

 
¹ Mention of trade names or commercial products in this publication is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the USDA.

Received for publication November 29, 2007. Accepted for publication April 3, 2008.

	REFERENCE

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCE

 
Ashton, W. L. G., M. Pattison, and K. C. Barnett. 1973. Light-induced eye abnormalities in turkeys and the turkey blindness syndrome. Res. Vet. Sci. 14:42–46.[Web of Science][Medline]

Borges, S. A., A. V. Fischer Da Silva, and A. Maiorka. 2007. Acid-base balance in broilers. Worlds Poult. Sci. J. 63:73–81.[Web of Science]

Bullis, K. L., G. H. Snoeyenbos, and H. van Roekel. 1950. A keratoconjunctivitis in chickens. Poult. Sci. 29:386–389.[Web of Science]

Burger, R. E., J. L. Osborne, and R. B. Banzett. 1974. Intrapulmonary chemoreceptors in Gallus domesticus: Adequate stimulus and functional localization. Respir. Physiol. 22:87–97.[CrossRef][Web of Science][Medline]

Burnett, R. W., and D. C. Noonan. 1974. Calculations and correction factors used in determination of blood pH and blood gases. Clin. Chem. 20:1499–1506.[Abstract]

Buyse, J., P. C. M. Simons, F. M. G. Boshouwers, and E. Decuypere. 1996. Effect of intermittent lighting, light intensity and source on the performance and welfare of broilers. Worlds Poult. Sci. J. 52:121–130.[CrossRef][Web of Science]

Carlile, I. 1984. Ammonia in poultry houses: A literature review. World’s Poult. Sci. J. 40:99–113.[CrossRef][Web of Science]

Charles, R. G., F. E. Robinson, R. T. Hardin, M. W. Yu, J. Feddes, and H. L. Classen. 1992. Growth, body composition, and plasma androgen concentration of male broiler chickens subjected to different regimens of photoperiod and light intensity. Poult. Sci. 71:1595–1605.[Web of Science][Medline]

Chui, P. S., J. K. Lauber, and A. Kinnear. 1975. Dimensional and physiological lesions in the chick eye as influenced by the light environment. Proc. Soc. Exp. Biol. Med. 148:1223–1228.[CrossRef][Medline]

Classen, H. L., C. Riddell, and F. E. Robinson. 1991. Effects of increasing photoperiod length on performance and health of broiler chickens. Br. Poult. Sci. 32:21–29.[CrossRef][Web of Science][Medline]

Cummings, T. S., J. D. French, and O. J. Fletcher. 1986. Ophthalmopathy in a broiler breeder flock reared in dark-out housing. Avian Dis. 30:609–612.[CrossRef][Web of Science][Medline]

Davenport, H. 1950. The ABC of Acid-Base Chemistry: The Elements of Physiological Blood-Gas Chemistry for Medical Students and Physicians. Univ. Chicago Press., Chicago, IL.

Davidovich, A., E. E. Bartley, and T. E. Chapman. 1977. Ammonia toxicity in cattle. II. Changes in carotid and jugular blood components associated with toxicity. J. Anim. Sci. 44:702–708.[Abstract/Free Full Text]

Eckert, R. 1988. Physical and chemical concepts. Pages pp. 8–34 in Animal Physiology. R. Eckert and D. Randall, ed. Freeman, New York, NY.

Elliott, R. J. 1984. Physicians and computers. Ektachem DT-60 analyzer. Physician’s Lead. 2:6–13.

Faddoul, G. P., and R. C. Ringrose. 1950. Avian keratoconjunctivitis. Vet. Med. (Praha) 45:492–493.

Gesell, R. 1925. The chemical regulation of respiration. Physiol. Rev. 5:551–595.[Free Full Text]

Gustin, P., B. Urbain, J. F. Prouvost, and M. Ansay. 1994. Effects of atmospheric ammonia on pulmonary hemodyamics and vascular permeability in pigs: Interaction with endotoxins. Toxicol. Appl. Pharmacol. 125:17–26.[CrossRef][Web of Science][Medline]

Harr, K. E. 2002. Clinical chemistry of companion avian species: A review. Vet. Clin. Pathol. 31:140–151.[Web of Science][Medline]

Hazelwood, R. L. 1986. Carbohydrate metabolism. Pages 303–325 in Avian Physiology. P. D. Sturkie, ed. Acad. Press, San Diego, CA.

Kristensen, H. H., and C. M. Wathes. 2000. Ammonia and poultry welfare: A review. World’s Poult. Sci. J. 56:235–245.[CrossRef][Web of Science]

Long, S. 1982. Acid-base balance and urinary acidification in birds. Comp. Biochem. Physiol. A 71:519–526.

Lloyd, W. E. 1970. Chemical and metabolic aspects of urea-ammonia toxicosis in cattle and sheep. PhD Diss. Iowa State Univ., Ames.

McFarlane, J. M., and S. E. Curtis. 1989. Multiple concurrent stressors in chicks. 3. Effect on plasma corticosterone and the heterophil:lymphocyte ratio. Poult. Sci. 68:522–527.[Web of Science][Medline]

Miles, D. M., S. L. Branton, and B. D. Lott. 2004. Atmospheric ammonia is detrimental to the performance of modern commercial broilers. Poult. Sci. 83:1650–1654.[Abstract/Free Full Text]

Miles, D. M., W. W. Miller, S. L. Branton, W. R. Maslin, and B. D. Lott. 2006. Ocular responses to ammonia in broiler chickens. Avian Dis. 50:45–49.[CrossRef][Web of Science][Medline]

NRC. 1994. Nutrient Requirements of Poultry. 9th ed. Natl. Acad. Sci., Washington, DC.

NRC. 1996. Guide for the Care and Use of Laboratory Animals. Natl. Acad. Press, Washington, DC.

NRC. 2003. Air Emissions from Animal Feeding Operations: Current Knowledge, Future Needs. Natl. Acad. Press, Washington, DC.

Olanrewaju, H. A., W. W. Miller, W. R. Maslin, J. P. Thaxton, J. L. Purswell, and S. L. Branton. 2007a. Interactive effects of ammonia and light intensity on ocular, fear, and leg health in broiler chickens. Int. J. Poult. Sci. 10:762–769.

Olanrewaju, H. A., J. P. Thaxton, W. A. Dozier III, and S. L. Branton. 2007b. Electrolyte diets, stress, and acid-base balance in chickens. Poult. Sci. 86:1363–1371.[Abstract/Free Full Text]

Olanrewaju, H. A., S. Wongpichet, J. P. Thaxton, W. A. Dozier III, and S. L. Branton. 2006. Stress and acid-base balance in chickens. Poult. Sci. 85:1266–1274.[Abstract/Free Full Text]

Quarles, C. L., and D. D. Caveny. 1979. Effect of air contaminants on performance and quality of broilers. Poult. Sci. 58:543–548.[Web of Science]

Rash, J. J., M. Muhrer, and R. A. Bloomfield. 1968. Identification of respiratory acidosis during ammonia toxicity. J. Anim. Sci. 26:1488. (Abstr.)

Reece, F. N., B. D. Lott, and J. W. Deaton. 1981. Low concentrations of ammonia during brooding decrease broiler weight. Poult. Sci. 60:937–940.[Web of Science]

Renden, J. A., S. F. Bilgili, R. J. Lien, and K. S. Kincaid. 1991. Live performance and yields of broilers provided various lighting schedules. Poult. Sci. 70:2055–2062.[Web of Science][Medline]

Roller, M. H., G. S. Riedemann, G. E. Romkema, and R. N. Swanson. 1982. Ovine blood chemistry values measured during ammonia toxicosis. Am. J. Vet. Res. 43:1068–1071.[Web of Science][Medline]

SAS Institute. 2004. SAS User’s Guide. Statistics. Version 9.1 ed. SAS Inst. Inc., Cary, NC.

Shideman, J. R., R. L. Evans, D. W. Bierer, and A. J. Quebbemann. 1981. Renal venous portal contribution to PAH and uric acid clearance in the chicken. Am. J. Physiol. 240:F46–F53.[Web of Science][Medline]

USDA. 2005. Agricultural Research Service Air Quality National Program Action Plan. http://www.ars.usda.gov/research/programs Accessed July 2, 2007.

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Olanrewaju, H. A. Articles by Branton, S. L. Search for Related Content PubMed PubMed Citation Articles by Olanrewaju, H. A. Articles by Branton, S. L.